WEDNESDAY, June 23 (HealthDay News) -- The introduction of gut bacteria into mice prone to developing arthritis and previously housed in germ-free conditions leads to rapid onset of the condition, according to research published online June 17 in Immunity.
Hsin-Jung Wu, Ph.D., of the Harvard Medical School in Boston, and colleagues analyzed data from K/BxN mice, which are susceptible to developing arthritis.
The researchers found that arthritis was reduced in mice under germ-free conditions, with reductions in serum autoantibody titers, germinal centers, and autoantibody-secreting cells and T helper 17 (Th17) cells in the spleen. In specific-pathogen-free mice, neutralizing interleukin-17 prevented the development of arthritis. Systemic deficiencies in germ-free mice were related to a loss of Th17 cells from the lamina propria of the small intestine, and introducing segmented filamentous bacteria into germ-free animals began the production of autoantibodies and rapidly led to arthritis.
"Because of the relatively high rate of discordance of human rheumatoid arthritis in monozygotic twins, the role of microbes in this disorder has been of great interest, although the conclusions have often been contentious. Only of late has some of the focus shifted to the potential influence of microbial commensals," the authors write. "Clearly, this is an area that merits further exploration, which will probably need to partner with studies on animal models to establish causality, permit mechanistic dissection, and allow preclinical evaluation of suggested therapeutic strategies."
Amgen Inc. provided mice used in the study.
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