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Discoveries

Intestinal flora may intensify MS

By Roger P. Smith, Ph.D.

Kasper, rear, and Ochoa-Repáraz study a mouse model of multiple sclerosis.

A team of DMS researchers has found that using antibiotics to reduce bacteria levels in the intestines of mice relieved symptoms associated with multiple sclerosis.

The interdisciplinary group, led by Lloyd Kasper, M.D., studies experimental autoimmune encephalomyelitis (EAE). This condition, which can be induced in mice, is widely regarded as the best experimental model of human multiple sclerosis (MS), an autoimmune condition that can cause a number of physical and cognitive problems. In MS, as in other autoimmune diseases, the immune system attacks its own tissues, either by producing antibodies that attack those tissues or by releasing molecules that cause inflammation and tissue damage. This can result in the loss of myelin, a fatty tissue that protects nerve fibers. In people with MS, patches of myelin and the underlying nerve fibers in the eyes, brain, and spinal cord are damaged or destroyed. About 400,000 Americans have MS, and about 2.5 million people worldwide suffer from the disease.

Role: Javier Ochoa-Repáraz, Ph.D., a research associate in Kasper's lab, used antibiotics to deplete the abundant bacteria that make their home in the intestines of mice—and humans. It is well established that the mucosal surfaces in the intestines play an important role in the immune system, but little is known about the role of all the bacteria in the intestines on the function of the immune system.

Ochoa-Repáraz gave mice with EAE a cocktail of antibiotics by mouth—thereby reducing the amount of bacteria in the intestines—and found that the treatment suppressed the development of EAE. When he gave the mice the same mix of antibiotics through an injection, there was no effect. So reducing the amount of bacteria in the intestines through the oral treatment promoted immune tolerance and hindered the development of this model of MS.

The causes of the effect are still not entirely clear, but the finding may represent an exciting new paradigm in the treatment of MS, and perhaps other autoimmune conditions, too.

Addendum: As noted in the article above, the research described here was conducted in mice, using a biological model of multiple sclerosis, not in humans and not on MS itself. So although the findings are of scientific interest, and could someday have clinical relevance, they are far from having any clinical application at the current time.


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