As reported by David Gutierrez in , researchers in a study conducted at the University of Nottingham point out that humans and gastrointestinal parasites might have coevolved in a way that the parasites actually help regulate the human immune system to prevent allergies.16 They believe that over the course of millions of years, gastrointestinal parasites have evolved the ability to suppress the human immune system as a survival mechanism. Because parasitic infestation has been so common throughout human evolutionary history, the human immune system has in turn evolved to compensate for this effect. This means that if the parasites are removed, the immune system may actually function too strongly, resulting in maladaptive immune responses such as asthma, allergies, and eczema. To test this concept the researchers studied over 1500 children in rural villages in Vietnam where parasitic infestation with hookworm is extremely common and allergies are not. Eradication of parasitic infection resulted in skyrocketing incidence of allergy, including dust mite sensitivity, supporting the hypothesis that parasites were modeling their immune response.
With issues such as the hygiene hypothesis, and the role of parasites in immune function in mind, gastroenterologist and researcher Dr. Joel Weinstock, originally at the University of Iowa and now Tufts University, has performed novel work with subjects with inflammatory bowel disease (IBD).17 IBD was unheard of before the 20th century. Beginning of 20th-century incidence is thought to be about 1:10,000 and is now 1:250. Similar data exist with the incidences of asthma, hay fever, DM, MS, and so on. Weinstock conducted various studies of IBD patients and treated them with the therapeutic parasite Trichuris suis, a porcine whipworm, which was an ideal choice as it only remains viable in the human GI tract for a short time and must be continually administered. The organism, when introduced into patients with IBD induced changes in regulatory T cell function, blocked T cell proliferation, altered cytokine production and expression of innate immunity, altered the intestinal flora, and generally produced a lessening of symptoms and severity of disease. Pharmaceutical agents are now being developed along these lines to treat IBD.
Molecular Mimicry, the Hygiene Hypothesis, Stealth Infections and Other Examples of Disconnect between Medical Research and the Practice of Clinical Medicine in Autoimmune Disease
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Researchers have now gone beyond establishing mere associations between the presence of various microbes and autoimmune disorders. Some have actually experimentally induced autoimmune disease by infecting animals with specific pathogens. Mazmanian et al. inoculated a wild-type mouse with the bacterium Helicobacter hepaticus to create an experimental mouse version of the autoimmune disorder inflammatory bowel disease (IBD).10 H. hepaticus activates Th17 cells, which release cytokines associated with inflammation, such as IL-17, which cause symptoms of the disease. They then introduced Bacteroides fragilis, expressing the polysaccharide A (PSA) to the gut of the animals, where the PSA molecule was taken up by dentritic cells and presented on their surface, activating CD4 T cells and regulatory T cells (Tregs). The Tregs release IL-10, which suppresses the inflammatory action of IL-17, alleviating the IBD in mice. In summary, the researchers induced autoimmune disease by introducing specific bacteria to the gut, and resolved it by introducing another, making a compelling argument for a causal relationship between the GI microbiota and autoimmune activity.
The hygiene hypothesis was first proposed to explain ..
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