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Your Rx: A Two-Week Infection with Intestinal Worms

Posted by Richard Conniff on July 19, 2012

More evidence that the world we live in is just too sanitary and that we need to spend more of our lives rolling in the dirt.

Type 1 diabetes has inexplicably become epidemic in this country, occurring 10-20 times more commonly than it did a century ago.

Now new research suggests an explanation.  Unlike us, people back then had intestinal worms to keep their immune systems in line.  Hard to imagine that as a good thing, but read the press release:

Short-term infection with intestinal worms may provide long-term protection against type I diabetes (TID), suggests a study conducted by William Gause, PhD, and colleagues at the University of Medicine and Dentistry of New Jersey-New Jersey Medical School. The research has been published in the journal Mucosal Immunology.

The incidence of TID—a form of the disease in which the body’s own immune cells attack the insulin-producing islet cells of the pancreas—is relatively low in developing countries. One explanation for this phenomenon is the prevalence of chronic intestinal worm infections, which dampen the self-aggressive T cells that cause diabetes and other autoimmune diseases. Understanding how T cells are tamed during worm infection could lead to new strategies to control these inflammatory diseases.

Dr. Gause’s team, including Pankaj Mishra, PhD, in his laboratory, and David Bleich, MD, now shows that a two-week infection with the intestinal worm H. polygyrus (cured using oral drugs) prompted T cells to produce the cytokines interleukin (IL)-4 and IL-10, which acted independently to provide lasting protection against TID in mice. A similar approach using eggs from another parasitic worm, Trichuris suis, is currently being tested in clinical trials in patients with Crohn’s disease and multiple sclerosis. The studies presented in this paper now provide potential mechanisms explaining the potency of parasite-induced control of inflammatory diseases.

You can read more here.   (And, as always, it mystifies me why the press release can’t include a simple link and citation for the research paper.  Here is the abstract, anyway.)

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