Excerpt:

Borrelia burgdorferi spirochetes cause Lyme disease, which can result in
severe clinical symptoms such as multiple joint inflammation and
neurological disorders. IFN-gamma 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-1beta has been linked to the generation
of IL-17-producing T cells, whereas caspase-1-mediated IL-18 is crucial for
IFN-gamma 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-gamma
and
IL-17 production after Borrelia stimulation. A lack of IL-1beta was
responsible for the defective IL-17 production, whereas IL-18 was crucial
for the IFN-gamma production. Caspase-1-dependent IL-33 played no role in
the Borrelia-induced production of IL-1beta, IFN-gamma 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 (c) 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.