Evasion of inflammasome activation by microbial pathogens
Tyler K. Ulland, … , Polly J. Ferguson, Fayyaz S. Sutterwala
Tyler K. Ulland, … , Polly J. Ferguson, Fayyaz S. Sutterwala
Published February 2, 2015
Citation Information: J Clin Invest. 2015;125(2):469-477. https://doi.org/10.1172/JCI75254.
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Review

Evasion of inflammasome activation by microbial pathogens

Abstract

Activation of the inflammasome occurs in response to infection with a wide array of pathogenic microbes. The inflammasome serves as a platform to activate caspase-1, which results in the subsequent processing and secretion of the proinflammatory cytokines IL-1β and IL-18 and the initiation of an inflammatory cell death pathway termed pyroptosis. Effective inflammasome activation is essential in controlling pathogen replication as well as initiating adaptive immune responses against the offending pathogens. However, a number of pathogens have developed strategies to evade inflammasome activation. In this Review, we discuss these pathogen evasion strategies as well as the potential infectious complications of therapeutic blockade of IL-1 pathways.

Authors

Tyler K. Ulland, Polly J. Ferguson, Fayyaz S. Sutterwala

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Figure 2

Bacterial effector molecule–mediated inhibition of the NLRC4 inflammasome.

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Bacterial effector molecule–mediated inhibition of the NLRC4 inflammasom...
Y. pseudotuberculosis YopK is secreted into the host cell through the T3SS; YopK interacts with the translocon structure of the T3SS and effectively masks it from recognition by NAIP/NLRC4. Y. pseudotuberculosis YopM directly inhibits caspase-1 by binding to its catalytically active site. Y. enterocolitica YopE and YopT inhibit caspase-1 activation through an unknown mechanism. P. aeruginosa ExoU and ExoS inhibit NLRC4 inflammasome and caspase-1 activation through an unknown mechanism.