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Infection and Immunity, August 2009, p. 3320-3327, Vol. 77, No. 8
0019-9567/09/$08.00+0     doi:10.1128/IAI.00100-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

The Caspase 1 Inflammasome Is Not Required for Control of Murine Lyme Borreliosis {triangledown}

Nengyin Liu,1 Alexia A. Belperron,1 Carmen J. Booth,2 and Linda K. Bockenstedt1*

Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520,1 Section of Comparative Medicine, Yale University School of Medicine, New Haven, Connecticut 065202

Received 27 January 2009/ Returned for modification 2 March 2009/ Accepted 21 May 2009

The contribution of the inflammasome to the development of immune responses and disease during infection with the Lyme disease spirochete, Borrelia burgdorferi, is not well defined. Host defense against the spirochete is severely impaired in mice deficient in the adaptor molecule myeloid differentiation antigen 88 (MyD88), which is required not only for Toll-like receptor-mediated responses but also for the production of the proforms of interleukin 1β (IL-1β) and IL-18. These cytokines are released in active forms after cleavage by the inflammasome-associated enzyme caspase 1. To investigate the contribution of the inflammasome to host defense against B. burgdorferi, we examined Lyme borreliosis in mice deficient in either caspase 1 or apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain (ASC), a molecule upstream of caspase 1 in the inflammasome signaling cascade. We found that caspase 1-deficient mice had a mild transient elevation in pathogen burden and a trend toward an increase in the prevalence of arthritis early in infection, but these differences resolved by day 14 postinfection. Caspase 1 deficiency had no effect on B. burgdorferi-induced humoral immunity, T-cell responses, or the abilities of macrophages to ingest and degrade spirochetes. The absence of the ASC protein had no effect on the control of the spirochete or the development of immune responses and disease. These findings reveal that the caspase 1 inflammasome is not critical to host defense against the extracellular pathogen Borrelia burgdorferi.

* Corresponding author. Mailing address: Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, P.O. Box 208031, New Haven, CT 06520. Phone: (203) 785-2453. Fax: (203) 785-7053. E-mail: linda.bockenstedt{at}yale.edu

{triangledown} Published ahead of print on 1 June 2009.

Editor: R. P. Morrison

Infection and Immunity, August 2009, p. 3320-3327, Vol. 77, No. 8
0019-9567/09/$08.00+0     doi:10.1128/IAI.00100-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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