Subversion of inflammasome activation and pyroptosis by pathogenic bacteria

Larissa D Cunha,Dario S Zamboni

doi:10.3389/fcimb.2013.00076

Larissa D Cunha, Dario S Zamboni

Open Access

https://doi.org/10.3389/fcimb.2013.00076

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Abstract

Activation of the inflammasome occurs in response to a notably high number of pathogenic microbes and is a broad innate immune response that effectively contributes to restriction of pathogen replication and generation of adaptive immunity. Activation of these platforms leads to caspase-1- and/or caspase-11-dependent secretion of proteins, including cytokines, and induction of a specific form of cell death called pyroptosis, which directly or indirectly contribute for restriction of pathogen replication. Not surprisingly, bona fide intracellular pathogens developed strategies for manipulation of cell death to guarantee intracellular replication. In this sense, the remarkable advances in the knowledge of the inflammasome field have been accompanied by several reports characterizing the inhibition of this platform by several pathogenic bacteria. Herein, we review some processes used by pathogenic bacteria, including Yersinia spp., Pseudomonas aeruginosa, Vibrio parahaemolyticus, Chlamydia trachomatis, Francisella tularensis, Shigella flexneri, Legionella pneumophila, and Coxiella burnetii to evade the activation of the inflammasome and the induction of pyroptosis.

Highlights

Host pattern recognition receptors (PRRs) are capable of sensing conserved microbial molecules, referred as Pathogen-Associated Molecular Patterns (PAMPs) as well as cellular disturbances, referred as Damage-Associated Molecular Patterns (DAMPs)
We review some processes used by pathogenic bacteria, including Yersinia spp., Pseudomonas aeruginosa, Vibrio parahaemolyticus, Chlamydia trachomatis, Francisella tularensis, Shigella flexneri, Legionella pneumophila, and Coxiella burnetii to evade the activation of the inflammasome and the induction of pyroptosis
Activation of intracellular PRRs belonging to the family of Nod-like receptors (NLRs) or the nucleic acid receptors AIM2 and IFI16 trigger a specific type of potentially pro-inflammatory, caspase-1-dependent cell death program known as pyroptosis (Cookson and Brennan, 2001; Lamkanfi and Dixit, 2012)

Summary

Subversion of inflammasome activation and pyroptosis by pathogenic bacteria

Activation of the inflammasome occurs in response to a notably high number of pathogenic microbes and is a broad innate immune response that effectively contributes to restriction of pathogen replication and generation of adaptive immunity. Activation of these platforms leads to caspase-1- and/or caspase-11-dependent secretion of proteins, including cytokines, and induction of a specific form of cell death called pyroptosis, which directly or indirectly contribute for restriction of pathogen replication. Bona fide intracellular pathogens developed strategies for manipulation of cell death to guarantee intracellular replication In this sense, the remarkable advances in the knowledge of the inflammasome field have been accompanied by several reports characterizing the inhibition of this platform by several pathogenic bacteria.

INTRODUCTION

Inflammasome subversion by pathogenic bacteria

MECHANISMS OF PYROPTOSIS INHIBITION BY BACTERIAL PATHOGENS

Pseudomonas aeruginosa

Inhibition of bacterial DNA release