Saturday, January 20, 2007

Parasites May Help Those With Multiple Sclerosis

Autoimmune diseases, such as Multiple Sclerosis have been on the rise in recent decades. Environmental factors could be the cause of this increase. One theory, states that an excessively germ-free environment may contribute to an increase in allergies, or a decline in infectious diseases may play a role in increasing autoimmune disease. The first study examining the relationship between parasite infections and MS in humans suggests that such infections may affect the immune response in a way that alters the course of MS.

Prior studies involving animals have shown that parasite infection can influence the course an autoimmune disease takes. These studies suggest that individuals with parasite infections have a diminished T cell response when unrelated antigens (foreign substances that generate an immune response) are present. The current study, conducted by Jorge Correale, M.D., and Mauricio Farez, B.Sc., of the Raúl Carrea Institute for Neurological Research in Buenos Aires, Argentina, involved 12 patients with MS who also had a parasite infection, 12 controls with MS who were uninfected, and twelve healthy individuals. The two groups of MS patients had a similar disease course. Patients had a neurological exam every three months and a brain MRI every six months, while immunological evaluations were conducted during the last twelve to eighteen months of the study. Patients were followed for an average of 4.6 years.

During the study period, there were three clinical relapses of MS in the infected group and 56 relapses in the uninfected group. Only two infected patients showed minimal Expanded Disability Status Score changes (EDSS is used to measure disability due to MS) that lasted less than three months, while the other ten had no changes in EDSS scores. In the uninfected group, eleven patients showed an overall increase in EDSS. Since MS involves an inflammatory response associated with the production of certain regulatory proteins known as cytokines, the number of cells producing cytokine suppressants was measured and found to be significantly higher in infected patients.

These findings provide evidence to support that an autoimmune response as a result of parasite infection can result in a decrease in the normal inflammatory response associated with MS. The authors note that evidence for production of regulatory T cells (which inhibit the immune response) in parasite infection is now emerging, which offers an explanation for the mechanism by which infected hosts exhibit an altered immune response that affects a secondary antigen, as was the case in the current study. "Thus, parasites may lead to increased regulatory T cell numbers or activity, either by generating new cells or by activating/expanding existing cells," they state.

Because parasites inhabit their hosts for long periods, they can develop molecules that generate strong anti-inflammatory responses, which enhance their survival. Further investigation is warranted in order to identify which molecules cause immune system effects that dampen the inflammatory reactions normally seen in autoimmune diseases. The authors conclude that "induction of a regulatory anti-inflammatory network generated by persistent parasite infections may offer a potential explanation for environment-related suppression of MS development in areas with low disease prevalence."

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