The Journal of Experimental Medicine
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Published online 22 May 2006 doi:10.1084/jem.20060206
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 6, 1407-1412
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BRIEF DEFINITIVE REPORT

 Role of the caspase-1 inflammasome in Salmonella typhimurium pathogenesis

Maria Lara-Tejero1, Fayyaz S. Sutterwala2,3, Yasunori Ogura3, Ethan P. Grant4, John Bertin4, Anthony J. Coyle4, Richard A. Flavell3, and Jorge E. Galán1

1 Section of Microbial Pathogenesis, 2 Section of Infectious Diseases, and 3 Section of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06536
4 Millenium Pharmaceuticals, Inc., Cambridge, MA 02139

CORRESPONDENCE Jorge E. Galán: jorge.galan{at}yale.edu

Caspase-1 is activated by a variety of stimuli after the assembly of the "inflammasome," an activating platform made up of a complex of the NOD-LRR family of proteins. Caspase-1 is required for the secretion of proinflammatory cytokines, such as interleukin (IL)-1ß and IL-18, and is involved in the control of many bacterial infections. Paradoxically, however, its absence has been reported to confer resistance to oral infection by Salmonella typhimurium. We show here that absence of caspase-1 or components of the inflammasome does not result in resistance to oral infection by S. typhimurium, but rather, leads to increased susceptibility to infection.

E.P. Grant and J. Bertin's present address is Synta Pharmaceuticals, Corp., Lexington, MA 02421.

A.J. Coyle's present address is Medimmune, Gaithersburg, MD 20878.


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