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Borrelia species induce inflammasome activation and IL-17 production through a caspase-1-dependent mechanism.

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Borrelia burgdorferi spirochetes cause
Lyme disease, which can result in severe clinical symptoms such as multiple joint inflammation and neurological disorders. IFN-? and IL-17 have been suggested to play an important role in the host defense against Borrelia, and in the immunopathology of
Lyme disease. The caspase-1-dependent cytokine IL-1? has been linked to the generation of IL-17-producing T cells, whereas caspase-1-mediated IL-18 is crucial for IFN-? production. In this study, we show by using knockout mice the role of inflammasome-activated caspase-1 in the regulation of cytokine responses by B. burgdorferi. Caspase-1-deficient cells showed significantly less IFN-? and IL-17 production after Borrelia stimulation. A lack of IL-1? was responsible for the defective IL-17 production, whereas IL-18 was crucial for the IFN-? production. Caspase-1-dependent IL-33 played no role in the Borrelia-induced production of IL-1?, IFN-? or IL-17. In conclusion, we describe for the first time the role of the inflammasome-dependent caspase-1 activation of cytokines in the regulation of IL-17 production induced by Borrelia spp. As IL-17 has been implicated in the pathogenesis of chronic
Lyme disease, these data suggest that caspase-1 targeting may represent a new immunomodulatory strategy for the treatment of complications of late stage
Lyme disease.

Copyright © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Eur J Immunol. 2011 Jan;41(1):172-81. doi: 10.1002/eji.201040385. Epub 2010 Dec 9. Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov’t

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