A team comprised of scientists at VIB, KU Leuven and UZ Leuven has made significant progress in uncovering the connection between psychological factors and the immune system. Their findings are based on an investigation of a massive drinking water contamination incident in Belgium in 2010, and are now published in the leading international medical journal Gut.
In December 2010, the Belgian communities of Schelle and Hemiksem in the province of Antwerp faced an outbreak of gastroenteritis, with more than 18,000 people exposed to contaminated drinking water. During the outbreak, VIB and KU Leuven set up a scientific task force to study the incident’s long-term effects, led by Guy Boeckxstaens (UZ Leuven / KU Leuven) and Adrian Liston (VIB / KU Leuven).
Seizing an unexpected opportunity
Adrian Liston (VIB/KU Leuven): “The water contamination in Schelle and Hemiksem was an ‘accidental experiment’ on a scale rarely possible in medical research. By following the patients from the initial contamination to a year after the outbreak we were able to find out what factors altered the risk of long-term complications.”
Anxiety and depression affect immune system
The scientists found that individual with higher levels of anxiety or depression prior to the water contamination developed gastrointestinal infections of increased severity. The same individuals also had an increased risk of developing the long-term complication of irritable bowel syndrome, with intermittent abdominal cramps, diarrhea or constipation a year after the initial contamination.
Guy Boeckxstaens (UZ Leuven / KU Leuven): “Irritable Bowel Syndrome is a condition of chronic abdominal pain and altered bowel movements. This is a common condition with large socio-economic costs, yet there is so much that still remains to be discovered about the causes. Our investigation found that that anxiety or depression alters the immune response towards a gastrointestinal infection, which can result in more severe symptoms and the development of chronic irritable bowel syndrome.”
Psychological factors key in preventing long-term complications
The study’s results provide valuable new insight into the cause of irritable bowel syndrome, and underscoring the connection between psychological factors and the immune system.
Adrian Liston (VIB/KU Leuven): “These results once again emphasize the importance of mental health care and social support services. We need to understand that health, society and economics are not independent, and ignoring depression and anxiety results in higher long-term medical costs.”
I remember studying the parasympathetic system in high school back in the 70’s. Basically we were taught that it exists and it balances the sympathetic system. Also recall we were taught that the nervous system and immune systems were separate, one did not “talk” to the other.
Kevin Tracey, a neurosurgeon based in New York, is a man haunted by personal events – a man with a mission. “My mother died from a brain tumor when I was five years old. It was very sudden and unexpected,” he says. “And I learned from that experience that the brain – nerves – are responsible for health.”
This background made him a neurosurgeon who thinks a lot about inflammation. He believes it was this perspective that enabled him to interpret the results of an accidental experiment in a new way.
In the late 1990s, Tracey was experimenting with a rat’s brain. “We’d injected an anti-inflammatory drug into the brain because we were studying the beneficial effect of blocking inflammation during a stroke,” he recalls. “We were surprised to find that when the drug was present in the brain, it also blocked inflammation in the spleen and in other organs in the rest of the body. Yet the amount of drug we’d injected was far too small to have got into the bloodstream and traveled to the rest of the body.”
After months puzzling over this, he finally hit upon the idea that the brain might be using the nervous system – specifically the vagus nerve – to tell the spleen to switch off inflammation everywhere.
It was an extraordinary idea – if Tracey was right, inflammation in body tissues was being directly regulated by the brain. Communication between the immune system’s specialist cells in our organs and bloodstream and the electrical connections of the nervous system had been considered impossible. Now Tracey was apparently discovering that the two systems were intricately linked.
…By taking the first detailed look at how one such parasite periodically assumes a new protein disguise during a long-term infection, new research at Rockefeller University challenges many assumptions about one of the best-known examples of this strategy, called antigenic variation, in the parasite that causes African sleeping sickness.
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Here’s how it works. Many animals, including humans, have immune systems capable of learning to recognize pathogens based on those pathogens’ antigens, usually proteins on their surface. After encountering an antigen, the immune system generates its own proteins called antibodies to target that antigen. By continually changing antigens, a pathogen evades those antibodies.
Resource May Help Identify Mechanisms of Immune-Related Diseases
WHAT:
An extensive database identifying immune traits, such as how immune cell function is regulated at the genetic level in healthy people, is reported by researchers from the National Institutes of Health (NIH) and their collaborators in the journal Cell. While many genetic risk factors have been linked to various diseases, including autoimmune disorders, how a genetic change causes susceptibility to a disease is not always clear. By studying healthy people, researchers from the National Institute of Allergy and Infectious Diseases (NIAID) Vaccine Research Center, part of the NIH, and colleagues from King’s College London have created a reference resource for other scientists.
The team analyzed blood samples collected from 669 female twins and developed a screening method that could differentiate approximately 78,000 subsets of immune cells, or immune traits. By using twins, the researchers identified which immune traits were most likely to be heritable and thus regulated at the genetic level. They selected 151 promising traits and performed a genome-wide approach to identify which, if any, genetic changes regulated a trait. They discovered 19 immune traits that were regulated by more than 240 genetic changes clustered within 11 areas of the human genome.
The results of this study have far-reaching implications, especially for researchers studying autoimmune disorders like multiple sclerosis, lupus, type 1 diabetes and inflammatory bowel disease. For example, genetic changes in the FCGR2 gene are known risk factors for several autoimmune disorders, including those just noted. However, it remains unclear how FCGR2 influences such a range of disorders. Now, researchers can use this new database to see how a change in FCGR2 or another gene affects components of the immune system and, subsequently, incorporate this information in the design of future studies.
ARTICLE:
M Roederer, L Quaye, M Mangino et al. The genetic architecture of the human immune system: a bioresource for autoimmunity and disease pathogenesis. Cell DOI: 10.1016/j.cell.2015.02.046 (2015).
WHO:
Mario Roederer, Ph.D., chief of the ImmunoTechnology Section in NIAID’s Vaccine Research Center, is available to discuss the findings.
Don’t think the article is advocating skip the annual flu shots!
Adults only really catch flu about twice a decade, suggests study
From the release
Adults over the age of 30 only catch flu about twice a decade, a new study suggests.
Flu-like illness can be caused by many pathogens, making it difficult to assess how often people are infected by influenza.
Researchers analysed blood samples from volunteers in Southern China, looking at antibody levels against nine different influenza strains that circulated from 1968 to 2009.
They found that while children get flu on average every other year, flu infections become less frequent as people progress through childhood and early adulthood. From the age of 30 onwards, flu infections tend to occur at a steady rate of about two per decade.
Dr Adam Kucharski, who worked on the study at Imperial College London before moving to the London School of Hygiene & Tropical Medicine, said: “There’s a lot of debate in the field as to how often people get flu, as opposed to flu-like illness caused by something else. These symptoms could sometimes be caused by common cold viruses, such as rhinovirus or coronavirus. Also, some people might not realise they had flu, but the infection will show up when a blood sample is subsequently tested. This is the first time anyone has reconstructed a group’s history of infection from modern-day blood samples.”
Dr Steven Riley, senior author of the study, from the Medical Research Council Centre for Outbreak Analysis and Modelling at Imperial, said: “For adults, we found that influenza infection is actually much less common than some people think. In childhood and adolescence, it’s much more common, possibly because we mix more with other people. The exact frequency of infection will vary depending on background levels of flu and vaccination.”
In addition to estimating the frequency of flu infection, the researchers, from the UK, the US and China, developed a mathematical model of how our immunity to flu changes over a lifetime as we encounter different strains of the virus.
Antibiotics significantly kill intestinal epithelium, the site of nutrient absorption, a part of our immune system and a place where other biological functions maintain human health.
From the 10 February 2015 Oregon State University press release
Researchers at Oregon State University have discovered that antibiotics have an impact on the microorganisms that live in an animal’s gut that’s more broad and complex than previously known.
The findings help to better explain some of the damage these medications can do, and set the stage for new ways to study and offset those impacts.
The work was published online in the journal Gut, in research supported by Oregon State University, the Medical Research Foundation of Oregon and the National Institutes of Health.
Researchers have known for some time that antibiotics can have unwanted side effects, especially in disrupting the natural and beneficial microbiota of the gastrointestinal system. But the new study helps explain in much more detail why that is happening, and also suggests that powerful, long-term antibiotic use can have even more far-reaching effects.
Scientists now suspect that antibiotic use, and especially overuse, can have unwanted effects on everything from the immune system to glucose metabolism, food absorption, obesity, stress and behavior.
The issues are rising in importance, since 40 percent of all adults and 70 percent of all children take one or more antibiotics every year, not to mention their use in billions of food animals. Although when used properly antibiotics can help treat life-threatening bacterial infections, more than 10 percent of people who receive the medications can suffer from adverse side effects.
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“Prior to this most people thought antibiotics only depleted microbiota and diminished several important immune functions that take place in the gut,” Morgun said. “Actually that’s only about one-third of the picture. They also kill intestinal epithelium. Destruction of the intestinal epithelium is important because this is the site of nutrient absorption, part of our immune system and it has other biological functions that play a role in human health.”
The research also found that antibiotics and antibiotic-resistant microbes caused significant changes in mitochondrial function, which in turn can lead to more epithelial cell death. That antibiotics have special impacts on the mitochondria of cells is both important and interesting, said Morgun, who was a co-leader of this study with Dr. Natalia Shulzhenko, a researcher in the OSU College of Veterinary Medicine who has an M.D. from Kharkiv Medical University.
Mitochondria plays a major role in cell signaling, growth and energy production, and for good health they need to function properly.
But the relationship of antibiotics to mitochondria may go back a long way. In evolution, mitochondria descended from bacteria, which were some of the earliest life forms, and different bacteria competed with each other for survival. That an antibiotic would still selectively attack the portion of a cell that most closely resembles bacteria may be a throwback to that ingrained sense of competition and the very evolution of life.
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Digestive dysfunction is near the top of the list, with antibiotic use linked to such issues as diarrhea and ulcerative colitis. But new research is also finding links to obesity, food absorption, depression, immune function, sepsis, allergies and asthma.
This research also developed a new bioinformatics approach named “transkingdom network interrogation” to studying microbiota, which could help further speed the study of any alterations of host microbiota interactions and antibiotic impact. This could aid the search for new probiotics to help offset antibiotic effects, and conceivably lead to systems that would diagnose a person’s microbiome, identify deficiencies and then address them in a precise and individual way.
The awe we feel when we’re in nature may help lower levels of pro-inflammatory proteins, a new study suggests (iStockphoto)
Taking in such spine-tingling wonders as the Grand Canyon, Sistine Chapel ceiling or Schubert’s “Ave Maria” may give a boost to the body’s defense system, according to new research from UC Berkeley.
Researchers have linked positive emotions – especially the awe we feel when touched by the beauty of nature, art and spirituality – with lower levels of pro-inflammatory cytokines, which are proteins that signal the immune system to work harder.
“Our findings demonstrate that positive emotions are associated with the markers of good health,” said Jennifer Stellar, a postdoctoral researcher at the University of Toronto and lead author of the study, which she conducted while at UC Berkeley.
While cytokines are necessary for herding cells to the body’s battlegrounds to fight infection, disease and trauma, sustained high levels of cytokines are associated with poorer health and such disorders as type-2 diabetes, heart disease, arthritis and even Alzheimer’s disease and clinical depression.
It has long been established that a healthy diet and lots of sleep and exercise bolster the body’s defenses against physical and mental illnesses. But the Berkeley study, whose findings were just published in the journal Emotion, is one of the first to look at the role of positive emotions in that arsenal.
Gut microbiomes from different people can contain similar microbial species, but different strains, as this cartoon illustrates.Dana C, Thomas
A large community of microorganisms calls the human digestive tract home. This dynamic conglomerate of microscopic life forms – the gut microbiome – is vital to how people metabolize various nutrients in their food, how their immune systems react to infection, and how they respond to various medications. Moreover, imbalances in the microbiome are thought to play a significant role in many human diseases.
The collection of species occupying the gut is known to be quite personalized, and people may differ considerably in the set of species they harbor. Now new research suggests that the differences between people may go even deeper. In a paper published Jan. 29 in Cell, researchers at the University of Washington show that even when people share microbes in common, the exact strains each carries might be very different.
“Knowing more about these strain-level variations,” said Elhanan Borenstein, the senior author of this paper and an associate professor of genome sciences at the University of Washington, “is crucial for understanding the complex relationship between the composition of the community of microbes living in the human gut and its influence on health and disease.”
Some people seem better than others at fighting the flu, and you might suspect they were born that way. A new study of twins, however, suggests otherwise.
In one of the most comprehensive analyses of immune function performed to date, researchers analyzed blood samples from 105 sets of healthy twins. They measured immune cell populations and their chemical messengers—204 parameters in all—before and after participants received a flu shot. Differences in three fourths of these parameters depended less on genetics than on environmental factors, such as diet and prior infections. Genetics had almost no effect on how well individuals responded to the flu vaccine, judged by antibodies produced against the injected material. And among identical twin siblings, who have the same genome, immune system features differed more strikingly within older twin pairs than in younger sets. The findings, published January 15 in Cell, argue that life habits and experiences shape our body’s defenses more than the DNA passed down from our parents.
Although prior twin studies had hinted that nonheritable factors contribute to some autoimmune disorders, such as multiple sclerosis, the recent analysis was one of the first to quantify genetic and environmental effects on the general immune system. “We were surprised by the degree of environmental influence on so many components,” says Mark Davis of Stanford University School of Medicine, senior author on the new study.
One finding was particularly striking. A single environmental factor—a past infection with common cytomegalovirus—affected 58 percent of the tested parameters. Whereas the results don’t show whether these changes produce an overall stronger or weaker immune response, they do indicate “cytomegalovirus has a really profound effect,” Davis says. The Epstein–Barr virus, another microbe that frequently infects people, had no such effect.
Electronic cigarettes, or e-cigarettes are growing in popularity among American adults, and while some states restrict their use by minors, nearly 1.8 million American middle and high school students reported using them one recent year, a federal study found.
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Manufacturers promote e-cigarettes as safer alternatives to conventional cigarettes and as tools for smoking cessation. Yet researchers point out that there is a dearth of scientific evidence regarding the effects of e-cigarette vapors on the lungs.
A laboratory study published in September suggests vapor from e-cigarettes may cause damage and raise the risk for respiratory infections among young people. In the lab, the vapor triggered a strong immune response in the epithelial cells of tissue samples donated by deceased children and the exposed cells appeared to be more vulnerable to infection by cold-causing rhinovirus, according to the research article, published in PLOS One. According to the study, even nicotine-free vapor increased the risk of infection.
HealthDay News reporter Dennis Thompson, who has been following the research on e-cigarette safety, took a look at the findings this month in a story posted on WebMD.
“Epithelial cells are the first line of defense in our airways,” the study’s lead author, Qun Wu, a lung disease researcher at National Jewish Health in Denver explains in Thompson’s article.
“They protect our bodies from anything dangerous we might inhale. Even without nicotine, this liquid can hurt your epithelial defense system and you will be more likely to get sick.”
Wu and his team placed the human cells in a sterile container in one end of a machine with an e-cigarette at the other end, Thompson notes. “The vapor spurred the release of IL-6, a signalling protein that promotes inflammation and an immune system response. This occurred whether or not the vapor contained nicotine, although nicotine appeared to slightly enhance the release of IL-6, the researchers said.”
An industry group representing e-cigarette manufacturers is stressing the limits of the study, pointing out that the tests involved cells in a lab, not actual e-cigarette users.
“Many in public health agree that the risks of vaping must always be considered in the context of the risks of cigarette smoking and traditional stop-smoking therapies,” Gregory Conley, president of the American Vaping Association observes in Thompson’s article.
UC Berkeley study finds self-worth key to diagnoses of psychopathologies
Donald Trump’s ego may be the size of his financial empire, but that doesn’t mean he’s the picture of mental health. The same can be said about the self-esteem of people who are living from paycheck to paycheck, or unemployed. New research from the University of California, Berkeley, underscores this mind-wallet connection.
UC Berkeley researchers have linked inflated or deflated feelings of self-worth to such afflictions as bipolar disorder, narcissistic personality disorder, anxiety and depression, providing yet more evidence that the widening gulf between rich and poor can be bad for your health.
The social self. (Photo credit: Wikipedia)
“We found that it is important to consider the motivation to pursue power, beliefs about how much power one has attained, pro-social and aggressive strategies for attaining power, and emotions related to attaining power,” said Sheri Johnson, a UC Berkeley psychologist and senior author of the study published in the journal Psychology and Psychotherapy: Theory, Research and Practice.
In a study of more than 600 young men and women conducted at UC Berkeley, researchers concluded that one’s perceived social status – or lack thereof – is at the heart of a wide range of mental illnesses. The findings make a strong case for assessing such traits as “ruthless ambition,” “discomfort with leadership” and “hubristic pride” to understand psychopathologies.
“People prone to depression or anxiety reported feeling little sense of pride in their accomplishments and little sense of power,” Johnson said. “In contrast, people at risk for mania tended to report high levels of pride and an emphasis on the pursuit of power despite interpersonal costs.”
Specifically, Johnson and fellow researchers Eliot Tang-Smith of the University of Miami and Stephen Chen of Wellesley College looked at how study participants fit into the “dominance behavioral system,” a construct in which humans and other mammals assess their place in the social hierarchy and respond accordingly to promote cooperation and avoid conflict and aggression. The concept is rooted in the evolutionary principle that dominant mammals gain easier access to resources for the sake of reproductive success and the survival of the species.
Studies have long established that feelings of powerlessness and helplessness weaken the immune system, making one more vulnerable to physical and mental ailments. Conversely, an inflated sense of power is among the behaviors associated with bipolar disorder and narcissistic personality disorder, which can be both personally and socially corrosive.
Source:Wyss Institute for Biologically Inspired Engineering at Harvard
Summary:
A non-surgical injection of programmable biomaterial that spontaneously assembles in vivo into a 3-D structure could fight and even help prevent cancer and also infectious disease such as HIV, scientists have demonstrated. Tiny biodegradable rod-like structures made from silica, known as mesoporous silica rods (MSRs), can be loaded with biological and chemical drug components and then delivered by needle just underneath the skin, they explain.
…
Their findings are reported in Nature Biotechnology.
“We can create 3D structures using minimally-invasive delivery to enrich and activate a host’s immune cells to target and attack harmful cells in vivo,” said the study’s senior author David Mooney, Ph.D., who is a Wyss Institute Core Faculty member and the Robert P. Pinkas Professor of Bioengineering at Harvard SEAS.
Tiny biodegradable rod-like structures made from silica, known as mesoporous silica rods (MSRs), can be loaded with biological and chemical drug components and then delivered by needle just underneath the skin. The rods spontaneously assemble at the vaccination site to form a three-dimensional scaffold, like pouring a box of matchsticks into a pile on a table. The porous spaces in the stack of MSRs are large enough to recruit and fill up with dendritic cells, which are “surveillance” cells that monitor the body and trigger an immune response when a harmful presence is detected.
An article by Sayer Ji, Activist Post, provides some thought-provocation and a lateral approach to a science, vaccination, that is currently in the news for its controversial issues concerning adverse reactions.
A groundbreaking study published this month in Nature challenges a century-old assumption about the innate pathogenicity of these extremely small, self-replicating particles known as viruses.
Titled, “An enteric virus can replace the beneficial function of commensal bacteria,” researchers found that an “enteric RNA virus can replace the beneficial function of commensal bacteria in the intestine.” Known as murine (mouse) noravirus (MNV), researchers found that infecting germ-free or antibiotic-treated mice infection with MNV “restored intestinal morphology and lymphocyte function without inducing overt inflammation and disease.”
The researchers found:
Importantly, MNV infection offset the deleterious effect of treatment with antibiotics in models of intestinal injury and pathogenic bacterial infection. These data indicate that eukaryotic viruses have the capacity to support intestinal homeostasis and shape mucosal immunity, similarly to commensal bacteria. Despite the commonly held belief that viruses are vectors of morbidity and mortality that must be vaccinated against in order to save us from inevitable harm and death, the new study dovetails with a growing body of research showing that our own genome is 80% viral in origin.
Summary: Scientists have uncovered a surprising way to reduce the brain damage caused by head injuries — stopping the body’s immune system from killing brain cells. A new study showed that in experiments on mice, an immune-based treatment reduced the size of brain lesions. The authors suggest that if the findings apply to humans, this could help prevent brain damage from accidents, and protect players of contact sports like football, rugby and boxing.
Story Source:
The above story is based on materials provided by BioMed Central. Note: Materials may be edited for content and length.
Journal Reference:
Richard P Tobin, Sanjib Mukherjee, Jessica M Kain, Susannah K Rogers, Stephanie K Henderson, Heather L Motal, M Rogers, Lee A Shapiro. Traumatic brain injury causes selective, CD74-dependent peripheral lymphocyte activation that exacerbates neurodegeneration. Acta Neuropathologica Communications, 2014; 2 (1): 143 DOI: 10.1186/s40478-014-0143-5
A comprehensive reference with helpful charts and personal stories. The guide covers major diseases, aging mental health, reproductive health, nutrition and alternative medicine. It also provices advice on common screening tests and immunizations you may need. (Previous item number: 107W)
Source: U.S. Department of Health and Human Services Released: 2008 Pages: 500
The time-course of an immune response begins with the initial pathogen encounter, (or initial vaccination) and leads to the formation and maintenance of active immunological memory. (Photo credit: Wikipedia)
In recent years, it has become increasingly clear that many diseases are triggered or maintained by changes in bacterial communities in the gut. However, the general view up into now has been rather simple: bacteria stimulate the immune system, leading to inflammation or autoimmune disorders in a single direction.
Now, in work published in Immunity, scientists led by Sidonia Fagarasan from the RIKEN Center for Integrative Medical Science in Japan have painted a more complex picture: the gut immune system does not simply prevent the influx of pathogens, but is actively involved in the maintenance of a rich and healthy community of gut bacteria. They propose that faults in the immune regulation lead to changes in the bacterial community that in turn feed back into the immune system.
In the study, the group demonstrated that the regulation by immune T cells of immunoglobulin A (IgA), an antibody that plays a key role in immunity in the gut, is critical for the maintenance of rich bacterial communities in mammal guts.
They began by studying mice with various immune deficiencies and attempted to restore the mice by providing the missing components. They monitored the bacterial communities in the mice’s guts with or without the reconstitutions and evaluated the flow of information between the immune system and bacteria. They discovered that the precise control of IgA production by regulatory T cells is critical for keeping a rich and balanced bacterial community.
To investigate how bacteria feed back to the host, they looked at germ-free mice (mice born and maintained sterile in special incubators) and young pups that had been transplanted with different bacterial communities (either by injection of bacteria or by painting the fur with fecal bacteria extracts from normal or immune-deficient mice). They discovered that the immune system “sees” and responds differently to different bacterial communities. Rich and balanced bacterial communities seem to be perceived as “self” and induce a quick maturation of the immune system and gut responses (induction of regulatory T cells and IgA), while a poor and unbalanced bacterial community is apparently perceived as “non-self” and induces responses aimed at eliminating it (T cells with inflammatory properties and IgG or IgE responses).
According to Sidonia Fagarasan, who led the work, “This study should have an impact on the way we understand immune-related disorders associated with bacteria dysbiosis in the gut. In order to reestablish a healthy state we need to interfere not only with the bacteria, by providing probiotics or through fecal transplantation, but also with the immune system, by correcting the faults caused either by inherited deficiencies or by aging.”
“It was surprising,” she continues, “to see how the reconstitution of T cell-deficient mice with a special regulatory T cell type leads to dramatic changes in gut bacterial communities. It was spectacular to see how the immune system perceives and reacts to different bacteria communities. It gives us hopes that with a better knowledge of the symbiotic relationships between the immune system and bacteria in the gut, we could intervene and induce modifications aiming to reestablish balance and restore health.”
Humans are able to smell sickness in someone whose immune system is highly active within just a few hours of exposure to a toxin, according to new research published in Psychological Science, a journal of theAssociation for Psychological Science.
According to researcher Mats Olsson of Karolinska Institutet in Sweden, there is anecdotal and scientific evidence suggesting that diseases have particular smells. People with diabetes, for example, are sometimes reported to have breath that smells like rotten apples or acetone.
Being able to detect these smells would represent a critical adaptation that would allow us to avoid potentially dangerous illnesses. Olsson wondered whether such an adaptation might exist already at an early stage of the disease.
“There may be early, possibly generic, biomarkers for illness in the form of volatile substances coming from the body,” explains Olsson.
To test this hypothesis, Olsson and his team had eight healthy people visit the laboratory to be injected with either lipopolysaccharide (LPS) — a toxin known to ramp up an immune response — or a saline solution. The volunteers wore tight t-shirts to absorb sweat over the course of 4 hours.
Importantly, participants injected with LPS did produce a noticeable immune response, as evidenced by elevated body temperatures and increased levels of a group of immune system molecules known as cytokines.
A separate group of 40 participants were instructed to smell the sweat samples. Overall, they rated t-shirts from the LPS group as having a more intense and unpleasant smell than the other t-shirts; they also rated the LPS shirt as having an unhealthier smell.
The association between immune activation and smell was accounted for, at least in part, by the level of cytokines present in the LPS-exposed blood. That is, the greater a participant’s immune response, the more unpleasant their sweat smelled.
Interestingly, in a chemical assay the researchers found no difference in the overall amount of odorous compounds between the LPS and control group. This suggests that there must have been a detectable difference in the composition of those compounds instead.
While the precise chemical compounds have yet to be identified, the fact we give off some kind of aversive signal shortly after the immune system has been activated is an important finding, the researchers argue. It grants us a better understanding of the social cues of sickness, and might also open up doors for understanding how infectious diseases can be contained.
Scientists at the Buck Institute for Research on Aging have promoted health and increased lifespan in Drosophila by altering the symbiotic, or commensal, relationship between bacteria and the absorptive cells lining the intestine. The research, appearing in the January 16, 2014 edition of Cell, provides a model for studying many of the dysfunctions that are characteristic of the aging gut and gives credence to the growing supposition that having the right balance of gut bacteria may be key to enjoying a long healthy life.
Even though recent research in humans has linked the composition of gut flora with diet and health in the elderly and the list of age-related diseases associated with changes in gut bacteria include cancer, diabetes, and inflammatory bowel disease, lead author and Buck faculty Heinrich Jasper, PhD, says there is no systematic understanding of how we go from having a young, healthy gut to one that is old and decrepit. “Our study explores age-related changes in the gut that include increased oxidative stress, inflammation, impaired efficiency of the immune response, and the over-proliferation of stem cells,” said Jasper. “It puts these changes into a hierarchical, causal relationship and highlights the points where we can intervene to rescue the negative results of microbial imbalance.”
Twelve ideas to help you stay healthy during flu season
The 2013 flu season has begun, and while it is still early in the season, cases have already been reported in the U.S. Winter gatherings can bring together people who are vulnerable to the cold & flu virus.
People who get together for the winter holidays can be exposed to viruses from other parts of the region and can pick up and spread the illness from wherever they’ve been. Here are some small, individual changes you can make lending to a healthy winter season.
Drink black or green tea with lemon and honey. Drinking hot tea while breathing in the steam stimulates the cilia – the hair follicles in the nose – to move out germs more efficiently. Lemon thins mucus and honey is antibacterial.
Consume enough protein. Diets that are too low in protein can deplete the immune system. The current recommendation for protein intake is at least 60 grams per day for adult women and at least 75 grams per day for adult men, depending on age, activity level and if they need to gain/lose weight.
Slowly exhale. When walking past a person who is sneezing or coughing, slowly exhale until you’re past them. This avoids you inhaling contaminated air.
Try Zinc lozenges. If you get a scratchy throat, zinc lozenges can relieve cold symptoms faster.
Eat your fruits and vegetables. Eating 5 or more fruits and vegetables each day will provide many vitamins and minerals necessary for your immune system to function properly. Try to choose more vegetables than fruit.
Sanitize your space. You can sanitize commonly touched items (cell phones, grocery carts, keyboards, gym equipment) to help the spread of germs. Remember, rhinoviruses causing cold & flu symptoms can live on surfaces for up to 48 hours!
Pamper your nose. The job of your nose is to filter allergens, bacteria, and viruses floating in the air. By using saline nasal rinses, you can help flush germs and clear secretions in your upper airway.
Consume enough water. The urge to drink water can decrease in colder months, but the need for water is still important. Consuming enough fluids will eliminate toxins from your lymph system which keeps your immune system functioning properly.
Sanitize your brushes. Think about the items you may reuse every day and consider cleaning or replacing them (cosmetics and make up brushes, toothbrushes, hair brushes, hand towels). A quick swipe of an alcohol wipe on a tube of lipstick or washing make up brushes in an antibacterial soap can support a healthy immune system.
Sleep. Research shows that adults need 7-8 hours of sleep to stimulate an immune response from our natural killer cells which are the cells that attack viruses.
Humidity. Dry air in the winter can cause your lips, mouth, & nose to become dry and cracked. Cracked skin can be an entry point for bacteria and viruses. Consider a humidifier to help keep moisture in the air.
Homemade Sani Wipes:
Fold or cut paper towels or napkins and put them into a wipe container. Use 1 1/2 cup of warm water, add 1 Tbsp. of coconut oil, and 1 tsp. of alcohol. Add 3 drops of lavender oil if you like. Then mix well and pour the mixture into the container of napkins to saturate them. Makes 2 containers.
Your health and wellness crew in WELLAWARE wish you a healthy winter season.
References
Patz, A. (2013, December). Live healthy. Health 27(10).
Revealing influenza’s truly insidious nature, Whitehead Institute scientists have discovered that the virus is able to infect its host by first killing off the cells of the immune system that are actually best equipped to neutralize the virus.
Confronted with a harmful virus, the immune system works to generate cells capable of producing antibodies perfectly suited to bind and disarm the hostile invader. These virus-specific B cells proliferate, secreting the antibodies that slow and eventually eradicate the virus. A population of these cells retains the information needed to neutralize the virus and takes up residence in the lung to ward off secondary infection from re-exposure to the virus via inhalation.
A new study by researchers at the Stanford University School of Medicine could help pinpoint ways to counter the effects of the antibiotics-driven depletion of friendly, gut-dwelling bacteria.
…
“Antibiotics open the door for these pathogens to take hold. But how, exactly, that occurs hasn’t been well understood,” Sonnenburg said.
In the first 24 hours after administration of oral antibiotics, a spike in carbohydrate availability takes place in the gut, the study says. This transient nutrient surplus, combined with the reduction of friendly gut-dwelling bacteria due to antibiotics, permits at least two potentially deadly pathogens to get a toehold in that otherwise more forbidding environment.
In the past decade or so, much has been learned about the complex microbial ecosystem that resides in every healthy mammal’s large intestine, including ours. The thousands of distinct bacterial strains that normally inhabit this challenging but nutrient-rich niche have adapted to it so well that we have difficulty living without them. They manufacture vitamins, provide critical training to our immune systems and even guide the development of our own tissues. Antibiotics decimate this gut-microbe ecosystem, which begins bouncing back within a few days but may take a month or more to regain its former numbers. And the ecosystem appears to suffer the permanent loss of some of its constituent bacterial strains.
It is thought that our commensal, or friendly, bacteria serve as a kind of lawn that, in commandeering the rich fertilizer that courses through our gut, outcompetes the less-well-behaved pathogenic “weeds.” It has also been suggested that our commensal bugs secrete pathogen-killing factors. Another theory holds that the disruption of our inner microbial ecosystem somehow impairs our immune responsiveness.
A set of proteins involved in the body’s natural defenses produces a large number of mutations in human DNA, according to a study led by researchers at the National Institutes of Health. The findings suggest that these naturally produced mutations are just as powerful as known cancer-causing agents in producing tumors.
The proteins are part of a group called apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like (APOBEC) cytidine deaminases. The investigators found that APOBEC mutations can outnumber all other mutations in some cancers, accounting for over two-thirds in some bladder, cervical, breast, head and neck, and lung tumors.
The scientists published their findings online July 14 in the journal Nature Genetics. Dmitry Gordenin, Ph.D., is corresponding author of the paper and a senior associate scientist at the National Institute of Environmental Health Sciences (NIEHS), part of NIH. He said scientists knew the main functions of APOBEC cytosine deaminases were to inactivate viruses that attack the body and prevent ancient viruses present in the human genome from moving around and causing disrupting mutations. Because they are so important to normal physiology, he and his collaborators were surprised to find a dark side to them — that of mutating human chromosomal DNA.
The study is a follow-up to one Gordenin and his group published in Molecular Cell in 2012, after they discovered APOBECs could generate clusters of mutations in some cancers.
AUDIO: Dmitry Gordenin, Ph.D., NIEHS, discusses results of research published July 14, 2013 in Nature Genetics.
“The presence of APOBEC clusters in the genome of tumor cells indicates that APOBEC enzymes could also have caused many mutations across the genome,” Gordenin said.
Gordenin’s team at NIEHS, comprised of scientists from the Chromosome Stability Group, headed by Michael Resnick, Ph.D., and the Integrative Bioinformatics Group, headed by David Fargo, Ph.D., took the 2012 research one step further by applying a modern data science approach.
The group collaborated with co-corresponding author Gad Getz, Ph.D., and other colleagues from the Broad Institute of MIT and Harvard, Cambridge, Mass. They looked for signs of genome-wide APOBEC mutagenesis in cancers listed in The Cancer Genome Atlas, a cancer database funded and managed by the National Cancer Institute and the National Human Genome Research Institute, both part of NIH.
Using APOBEC’s distinctive DNA mutational signature, they examined approximately 1 million mutations in 2,680 cancer samples, and found that, in some tumors, nearly 70 percent of mutations in a given specimen resulted from APOBEC mutagenesis. The mutation pattern, which appeared in clusters and individual mutations, could affect many cancer-associated genes.
Steven Roberts, Ph.D., a postdoctoral fellow who works with Gordenin, is first author on both studies. He explained that since APOBECs are regulated by the immune system, which is responsive to many environmental factors, he believes there may be a significant environmental component to APOBEC mutagenesis.
“We hope that determining the environmental link to these mutations will lead to viable cancer prevention strategies,” Roberts said.
In upcoming work, he and Gordenin plan to address why APOBEC mutagenesis appears in some cancer types and not others.
The gut mucosa is the largest and most dynamic immunological environment of the body. It hosts the body’s largest population of immune cells. It is often the first point of pathogen exposure and many microbes use it as a beachhead into the rest of the body.
The gut immune system therefore needs to be ready to respond to pathogens but at the same time it is constantly exposed to innocuous environmental antigens, food particles and commensal microflora which need to be tolerated.
Misdirected immune responses to harmless antigens are the underlying cause of food allergies and debilitating conditions such as inflammatory bowel disease. This animation introduces the key cells and molecular players involved in gut immunohomeostasis and disease.
Nature Immunology in collaboration with Arkitek Studios have produced an animation unraveling the complexities of mucosal immunology in health and disease:
Researchers may soon be able to add yet another item to the list of exercise’s well-documented health benefits: A preliminary study suggests that when cancer survivors exercise for several weeks after they finish chemotherapy, their immune systems remodel themselves to become more effective, potentially fending off future incidents of cancer. The finding may help explain why exercise can significantly reduce the chances of secondary cancers in survivors or reduce the chances of cancer altogether in people who have never had the disease…
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“What we’re suggesting is that with exercise, you might be getting rid of T cells that aren’t helpful and making room for T cells that might be helpful,” Bilek says.
She adds that this finding highlights the importance of exercise for all, including those with cancer and cancer survivors. These two populations might benefit especially from the heightened “cancer surveillance” — the ability of the immune system to seek out and destroy budding cancers — that this study suggests exercise brings, Bilek explains.
“There’s a litany of positive benefits from exercise,” Bilek says. “If exercise indeed strengthens the immune system and potentially improves cancer surveillance, it’s one more thing we should educate patients about as a reason they should schedule regular activity throughout their day and make it a priority in their lives.”
Many scientists now regard human bodies as “supra-organisms”, collections of communities made up of human and microbial cells coexisting in a whole that is more than the sum of its parts.
Scientists working on a huge project that has mapped all the different microbes that live in and on a healthy human body have made a number of remarkable discoveries, including the fact that harmful bacteria can live in healthy bodies and co-exist with their host and other microbes without causing disease.
This week sees the publication of several papers from the Human Microbiome Project (HMP), including two in Nature and two inPLoS ONE.
The Microbiome
The microbiome is the sum of all the microbes that colonize the body: it comprises trillions of microorganisms that outnumber human cells by 10 to 1. The microbes inhabit every nook and cranny of the body, and most of the time the relationship is a friendly one, because they help digest food, strengthen the immune system and fight off dangerous pathogens.
Colorado University (CU)-Boulder Associate Professor Rob Knight of the BioFrontiers Institute is co-author on the two Nature papers. He told the press that the microbiome may only make up 1 to 3% of human body mass, but it plays a key role in human health.
One of the fascinating features of the microbiome is that different body sites have different communites of microorganisms that are as different from each other as the differences between microbial communities in oceans and deserts.
Knight said:
“By better understanding this microbial variation we can begin searching for genetic biomarkers for disease.”
Another of the curious features the HMP has discovered is that even healthy people carry low levels of harmful bacteria, but as long as the body remains healthy, they don’t cause disease, they just coexist alongside beneficial microbes. …
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The HMP researchers established that more than 10,000 microbial species inhabit the human “ecosystem”. Knight said they believe they have now found between 81 and 99% of all genera of microorganisms in healthy adult Americans.
One of the key findings was the stark differences in microbial communities across the human body. For instance, the microbial communities that live on the teeth are different from those in saliva. …
…Another interesting discovery is that of the genes that influence human metabolism, most of them are in the microbiome and not in the human genome…
…gut bacteria do more than break down food and its constituents like proteins, fats and carbohydrates, they also produce beneficial compounds like vitamins and anti-inflammatories.
The billions of bugs in our guts have a newfound role: regulating the immune system and related autoimmune diseases such as rheumatoid arthritis, according to researchers at Mayo Clinic and the University of Illinois at Urbana-Champaign.
Larger-than-normal populations of specific gut bacteria may trigger the development of diseases like rheumatoid arthritis and possibly fuel disease progression in people genetically predisposed to this crippling and confounding condition, say the researchers, who are participating in the Mayo Illinois Alliance for Technology Based Healthcare.
The study is published in the April 2012 issue of PLoS ONE.
“A lot of people suspected that gut flora played a role in rheumatoid arthritis, but no one had been able to prove it because they couldn’t say which came first — the bacteria or the genes,” says senior author Veena Taneja, Ph.D., a Mayo Clinic immunologist. “Using genomic sequencing technologies, we have been able to show the gut microbiome may be used as a biomarker for predisposition.”…
…Researchers found that hormones and changes related to aging may further modulate the gut immune system and exacerbate inflammatory conditions in genetically susceptible individuals…
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“The gut is the largest immune organ in the body,” says co-author Bryan White, Ph.D., director of the University of Illinois’ Microbiome Program in the Division of Biomedical Sciences and a member of the Institute for Genomic Biology. “Because it’s presented with multiple insults daily through the introduction of new bacteria, food sources and foreign antigens, the gut is continually teasing out what’s good and bad.”
The gut has several ways to do this, including the mucosal barrier that prevents organisms — even commensal or “good” bacteria — from crossing the lumen of the gut into the human body. However, when commensal bacteria breach this barrier, they can trigger autoimmune responses. The body recognizes them as out of place, and in some way this triggers the body to attack itself, he says….
Exciting new data presented at the International Liver Congress™ 2012 shows the gut microbiota’s causal role in the development of diabetes and non-alcoholic fatty liver disease (NAFLD), independent of obesity.(1) Though an early stage animal model, the French study highlights the possibility of preventing diabetes and NAFLD with gut microbiota transplantation – the engrafting of new microbiota, usually through administering faecal material from a healthy donor into the colon of a diseased recipient.(2) …
…”This study shows that different microbiota cause different metabolic responses in animals. By implanting microbiota from healthy mice, the study authors prevented the development of liver inflammation and insulin resistance, both indications of liver disease and diabetes. Thus, gut microbiota transplants could have a therapeutic role in the development of these diseases.”
The RR mice also showed lower levels of microorganisms than usually found in the healthy gut. Lachnospiraceae was identified as the species most important in developing fatty liver and insulin resistance.
At present, the intestinal microbiota is considered to constitute a “microbial organ”: one that has pivotal roles in the body’s metabolism as well as immune function. Therefore transplantation aims to restore gut functionality and re-establish a certain state of intestinal flora.
The Ecosystem Inside (From the Magazine Discover Mar2011, Vol. 32 Issue 2, p35-39, 5p)
[Not directly available online..Check with your library…I was able to get the full text through my hometown’s public library Web pages] Abstract:
The article focuses on research into the human microbiome, made up of the up to 200 trillion microbes–including bacteria, fungi, and viruses–that live primarily in the human gut and form their own ecology. Pediatrician Patrick Seed and biologist Rob Jackson are collaborating on the Preemie Microbiome Project at Duke University, aiming to understand the role of microbiome species in infant health.
[Article excerpts]
“The classical view of infectious disease is that a single organism invades and produces an infection,” Seed says. “But then we found that certain diseases, like irritable bowel syndrome, seem , to be caused by imbalances in the organisms that communicate with the host. So then people asked, ‘Why is this not the case for many other states of human health?'” Preliminary work by other groups, similarly made up of both biomedical researchers and microbial ecologists, suggests that imbalances in the microbiome might also be linked to allergies, diabetes, and obesity.The partnership between ecologists and biomedical researchers is characteristic of how things work in the relatively new but burgeoning field of microbiome studies. Vanja Klepac-Ceraj, a microbial ecologist by training and an assistant research investigator at the Forsyth Institute in Cambridge, Massachusetts, has helped organize symposia with ecologists and biomedical researchers giving joint.talks on the ecology of disease. “Biomedical scientists understand disease, so they know where the problem lies within the body,” she says. “Ecologists understand complex systems and the interaction of many organisms….
…MICROBIOME STUDIES RUN DIRECTLY AGAINST THE NOTION IN THE minds of most people — even many researchers — that microbes are linked to disease, not to health. And of course not all microorganisms are benign. Infants in particular are susceptible to a number of diseases caused by gastrointestinal bacteria, including sepsis, chronic diarrhea, and necrotizing enterocolitis, an infection of the intestinal lining that is one of the leading causes of death in premature babies. Antibiotics have long been the first option in fighting these dangerous microbes, but many researchers are troubled by modern medicine’s heavy reliance on them. After all, many pathogens found within the human microbiome are harmless or even beneficial. “There is Staphylococcus and E. coli in all of us, but they don’t always cause problems,” Jackson says. “It’s the balance that is important. A more normal population of microbes in the gut can offset the bad players”…
…In another animal microbiome experiment, Jeffrey Gordon, a biologist at Washington University in St Louis, took a suite of microbesfrom the guts of both obese and lean mice and transplanted them into the guts of microbe-free mice. The mice that received the microbiomes of the obese mice gained significantly more weight than did the mice with the lean-mouse microbiomes. The results were the same regardless of whether the obesity of the donor mice was due to genetics or diet. Although caloric intake is still the most important factor in obesity, Gordon’s research suggests that the microbiome may play a significant role by affecting the ability to extract energy from food and to deposit that energy as fat:
Researchers hope to achieve similarly dramatic results in humans next. A critical step in making this happen is deciphering how microbes communicate. “The establishment of healthy microbial communities almost certainly requires chemical messaging between the species present in the human host,” says Texas A&M University biochemist Paul Straight, who studies interactions among bacteria. Microbes can use chemical signals, including small molecules, proteins, and DNA, to encourage neighboring organisms to grow or to tell them to stop growing. If researchers can capture and understand these molecular exchanges, they might be able to produce a kind of phrase book of chemical reactions. Such information could then be used to initiate this kind of molecular conversation on command, with an eye toward promoting the growth of helpful microbes or stunting harmful ones.
Specially packaged mixtures of microbes, known as probiotics, may also prove useful for balancing microbes in the gut (See “Bugs for Breakfast,” opposite), Probiotics are now generally sold as health food supplements, and many of them are promoted as magic bullets that can improve metabolism or bolster immunity. Since they are as yet unregulated by the FDA, though, it is impossible for the consumer to know exactly what is inside; labels on over-the-counter products can be deceptive. Scientists who have tested them have often found something quite different from what the product promises. Nevertheless, carefully regulated probiotics, which introduce nonpathogenic competitors to disease, could be effective at balancing the gut microbiome…..
Rhesus macaques on Qianling Shan in the outskirts of Guiyang. Norsk (bokmål)â¬: Rhesusmakaker på Qianling Shan i utkanten av Guiyang. (Photo credit: Wikipedia)
If a monkey’s social status changes, her immune system changes along with it say researchers who conducted the study with rhesus macaques at the Yerkes National Primate Research Center. This finding may have implications for how the stress of low socioeconomic status affects human health and how individuals’ bodies adapt after a shift in their social environment. The results are published this week in the Proceedings of the National Academy of Sciences Early Edition…
From the 3 March 2012 article at Science News Daily
Depression is common enough — afflicting one in ten adults in the United States — that it seems the possibility of depression must be “hard-wired” into our brains. This has led biologists to propose several theories to account for how depression, or behaviors linked to it, can somehow offer an evolutionary advantage
Some previous proposals for the role of depression in evolution have focused on how it affects behavior in a social context. A pair of psychiatrists addresses this puzzle in a different way, tying together depression and resistance to infection. They propose that genetic variations that promote depression arose during evolution because they helped our ancestors fight infection….
“The basic idea is that depression and the genes that promote it were very adaptive for helping people — especially young children — not die of infection in the ancestral environment, even if those same behaviors are not helpful in our relationships with other people,” Raison says.
Infection was the major cause of death in humans’ early history, so surviving infection was a key determinant in whether someone was able to pass on his or her genes. The authors propose that evolution and genetics have bound together depressive symptoms and physiological responses that were selected on the basis of reducing mortality from infection. Fever, fatigue/inactivity, social avoidance and anorexia can all be seen as adaptive behaviors in light of the need to contain infection, they write.
The theory provides a new explanation for why stress is a risk factor for depression. The link between stress and depression can be seen as the byproduct of a process that preactivates the immune system in anticipation of a wound, they write….
Genetics has provided surprising insights into why vaccines used in both the UK and US to combat serious childhood infections can eventually fail. The study, recently published in Nature Genetics, which investigates how bacteria change their disguise to evade the vaccines, has implications for how future vaccines can be made more effective…
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n spite of the success of the vaccine programmes, some pneumococcal strains managed to continue to cause disease by camouflaging themselves from the vaccine. In research funded by the Wellcome Trust, scientists at the University of Oxford and at the Centers for Disease Control and Prevention in Atlanta studied what happened after the introduction of this vaccine in the US. They used the latest genomic techniques combined with epidemiology to understand how different serotypes of the pneumococcus bacteria evolve to replace those targeted by the initial vaccine.
The researchers found bacteria that had evaded the vaccine by swapping the region of the genome responsible for making the polysaccharide coating with the same region from a different serotype, not targeted by the vaccine. This effectively disguised the bacteria, making it invisible to the vaccine….
IMAGE: This electron microscope image shows yellow particles of a mouse leukemia virus named Friend virus emerging or “budding ” out of an infected white blood cell known as a T-cell. By…
SALT LAKE CITY, Feb. 6, 2012 – University of Utah biologists found new evidence why mice, people and other vertebrate animals carry thousands of varieties of genes to make immune-system proteins named MHCs – even though some of those genes make us susceptible to infections and to autoimmune diseases.
“Major histocompatibility complex” (MHC) proteins are found on the surface of most cells in vertebrate animals. They distinguish self from foreign, and trigger an immune response against foreign invaders. MHCs recognize invading germs, reject or accept transplanted organs and play a role in helping us smell compatible mates.
“This study explains why there are so many versions of the MHC genes, and why the ones that cause susceptibility to diseases are being maintained and not eliminated,” says biology Professor Wayne Potts. “They are involved in a never-ending arms race that causes them, at any point in time, to be good against some infections but bad against other infections and autoimmune diseases.”
By allowing a disease virus to evolve rapidly in mice, the study produced new experimental evidence for the arms race between genes and germs – known technically as “antagonistic coevolution.” The findings will be published online the week of Feb. 6, 2012, in the journal Proceedings of the National Academy of Sciences.
Potts, the senior author, ran the study with first author and former doctoral student Jason Kubinak, now a postdoctoral fellow in pathology. Other co-authors were biology doctoral student James Ruff, biology undergraduate C. Whitney Hyzer and Patricia Slev, a clinical assistant professor of pathology. The research was funded by the National Science Foundation and the National Institute of Allergy and Infectious Diseases.
More than 32 million people in the United States have autoantibodies, which are proteins made by the immune system that target the body’s tissues and define a condition known as autoimmunity, a study shows. The first nationally representative sample looking at the prevalence of the most common type of autoantibody, known as antinuclear antibodies (ANA), found that the frequency of ANA is highest among women, older individuals, and African-Americans. The study was conducted by the National Institute of Environmental Health Sciences (NIEHS), part of the National Institutes of Health. Researchers in Gainesville at the University of Florida also participated.
Earlier studies have shown that ANA can actually develop many years before the clinical appearance of autoimmune diseases, such as type 1 diabetes, lupus, and rheumatoid arthritis. ANA are frequently measured biomarkers for detecting autoimmune diseases, but the presence of autoantibodies does not necessarily mean a person will get an autoimmune disease. Other factors, including drugs, cancer, and infections, are also known to cause autoantibodies in some people…
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“The peak of autoimmunity in females compared to males during the 40-49 age bracket is suggestive of the effects that the hormones estrogen and progesterone might be playing on the immune system,” said Linda Birnbaum, Ph.D., director of NIEHS and an author on the paper.
The paper also found that the prevalence of ANA was lower in overweight and obese individuals than persons of normal weight. “This finding is interesting and somewhat unexpected,” said Edward Chan, Ph.D., an author on the study and professor of the Department of Oral Biology at the University of Florida.
“It raises the likelihood that fat tissues can secrete proteins that inhibit parts of the immune system and prevent the development of autoantibodies, but we will need to do more research to understand the role that obesity might play in the development of autoimmune diseases,” said Minoru Satoh, M.D., Ph.D., another author on the study and associate professor of rheumatology and clinical immunology at the University of Florida….
From the 21 December 2011 Science News Today article
Scientists of the Institute of Tropical Medicine (ITG) discovered a parasite that not only had developed resistance against a common medicine, but at the same time had become better in withstanding the human immune system. With some exaggeration: medical practice helped in developing a superbug. For it appears the battle against the drug also armed the bug better against its host.
“To our knowledge it is the first time such a doubly armed organism appears in nature,” says researcher Manu Vanaerschot, who obtained a PhD for his detective work at ITG and Antwerp University. “It certainly makes you think.”…
High diversity and a variety of bacteria in the gut protect children against allergies as opposed to some individual bacterial genera. These are the findings of a comprehensive study of intestinal microflora (gut flora) in allergic and healthy children, which was conducted at Linköping University in Sweden.
One hypothesis is that our immune system encounters too few bacteria during childhood, which explains the increasing proportion of allergic children. However it has been difficult to substantiate the hypothesis scientifically.
“We conducted the study in collaboration with Karolinska Institute and the KTH Royal Institute of Technology which substantiates the so-called hygiene hypothesis. Children acquire intestinal microflora from their environment, and in our society they are probably exposed to insufficient bacteria that are necessary for the immune system to mature”, says Thomas Abrahamsson, paediatric physician and a researcher at Linköping University….
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It is the composition of intestinal microflora during the first weeks of life that show signs of being critical to the immune system’s development. In the absence of sufficient stimuli from many different bacteria, the system may overreact against harmless antigens in the environment, such as foods. The risk of developing asthma at school age for children afflicted by these allergies is five to six times higher.
Allergy (Medline Plus) with links to overviews, news items, diagnosis/treatments, prevention, research items, alternative therapies, tutorials, videos, and more
“One of the most comprehensive studies to date of the microbes that are found in extremely low-birthweight infants found that hard-to-treat Candida fungus is often present, as well as some harmful bacteria and parasites
Researchers at the Duke University Medical Center and Nicholas School of the Environment looked at the microbes in 11 premature infants and found much less diversity than in full-term infants.
“The babies’ guts were taken over by microbes we know are dangerous if they get into the blood,” said senior author Patrick Seed, MD, PhD, assistant professor of pediatrics at Duke. “Even after the babies were no longer on antibiotics, healthier bacteria didn’t appear in the babies very quickly. This may be one reason why premature babies are so vulnerable to infections.”……
A stem cell that can morph into a number of different tissues is proving a natural protector, healer and antibiotic maker, researchers at Case Western Reserve University and their peers have found.
Mesenchymal stem cells reaped from bone marrow had been hailed as the key to growing new organs to replace those damaged or destroyed by violence or disease, but have failed to live up to the billing.
Instead, scientists who’d been trying to manipulate the cells to build replacement parts have been finding the cells are innately potent antidotes to a growing list of maladies.
The findings are summarized in the July 8 issue of Cell Stem Cell.
The cell, referred to as an MSC, “is a drugstore that functions at the local site of injury to provide all the medicine that site requires for its successful regeneration,” said Arnold Caplan, professor of biology at Case Western Reserve, and lead author of the paper.
European researchers report rural living less likely to lead to atopic dermatitis for infants
Childhood exposure to germs in the environment strengthens their immune system, according to current scientific evidence. (See Immune System (http://www.niaid.nih.gov/topics/immuneSystem/Pages/immunity.aspx) by the National Institute of Allergy and Infectious Diseases [NIAID])
Now it seems that the environment not only confers immunity through not only interacting with a child’s immune system after birth, but before birth.
WEDNESDAY, Dec. 8 (HealthDay News) — The children of mothers who were around farm animals and cats during pregnancy are less likely to develop atopic dermatitis in their first two years of life, new European research shows.
Atopic dermatitis (also called atopic eczema) is a chronic and painful inflammation of the skin that frequently occurs in childhood. The condition affects up to 20 percent of children in industrialized countries and is one of the most common childhood skin diseases….
….Along with the first finding, the researchers also identified two genes associated with a child’s reduced risk of developing atopic dermatitis in the first two years of life.
The findings support the theory that a gene-environment interaction with a child’s developing immune system influences the development of atopic dermatitis, said the researchers.
From the 9 February 2012 Medical News Today article
Immunological diseases, such as eczemaand asthma, are on the increase in westernised society and represent a major challenge for 21st century medicine. A new study has shown, for the first time, that growing up on a farm directly affects the regulation of the immune system and causes a reduction in the immunological responses to food proteins. …
…Dr Marie Lewis, Research Associate in Infection and Immunity at the School of Veterinary Sciences, who led the research, said: “Many large-scale epidemiological studies have suggested that growing up on a farm is linked to a reduced likelihood of developing allergic disease. However, until now, it has not been possible to demonstrate direct cause and effect: does the farm environment actively protect against allergies, or are allergy-prone families unlikely to live on farms?” ,,,
MONDAY, Nov. 1 (HealthDay News) — There may not be a cure for the common cold, but people who exercise regularly seem to have fewer and milder colds, a new study suggests.
In the United States, adults can expect to catch a cold two to four times a year, and children can expect to get six to 10 colds annually. All these colds sap about $40 billion from the U.S. economy in direct and indirect costs, the study authors estimate.
But exercise may be an inexpensive way to put a dent in those statistics, the study says.
“The physically active always brag that they’re sick less than sedentary people,” said lead researcher David C. Nieman, director of the Human Performance Laboratory at the Appalachian State University, North Carolina Research Campus, in Kannapolis, N.C.
“Indeed, this boast of active people that they are sick less often is really true,” he asserted.
The report is published in the Nov. 1 online edition of the British Journal of Sports Medicine.
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This blog presents a sampling of health and medical news and resources for all. Selected articles and resources will hopefully be of general interest but will also encourage further reading through posted references and other links. Currently I am focusing on public health, basic and applied research and very broadly on disease and healthy lifestyle topics.
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