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Review
. 2016 Feb:29:56-62.
doi: 10.1016/j.mib.2015.11.001. Epub 2015 Nov 27.

Yersinia versus host immunity: how a pathogen evades or triggers a protective response

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Review

Yersinia versus host immunity: how a pathogen evades or triggers a protective response

Lawton K Chung et al. Curr Opin Microbiol. 2016 Feb.

Abstract

The human pathogenic Yersinia species cause diseases that represent a significant source of morbidity and mortality. Despite this, specific mechanisms underlying Yersinia pathogenesis and protective host responses remain poorly understood. Recent studies have shown that Yersinia disrupt cell death pathways, perturb inflammatory processes and exploit immune cells to promote disease. The ensuing host responses following Yersinia infection include coordination of innate and adaptive immune responses in an attempt to control bacterial replication. Here, we highlight current advances in our understanding of the interactions between the pathogenic yersiniae and host cells, as well as the protective host responses mobilized to counteract these pathogens. Together, these studies enhance our understanding of Yersinia pathogenesis and highlight the ongoing battle between host and microbe.

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Figures

Figure 1
Figure 1. Yersinia vs. host immunity
(a) Evasion of host signaling pathways by the type III secretion system. YpkA association with actin monomers targets actin-regulating proteins to inhibit phagocytosis. In neutrophils, delivery of YopH leads to dephosphorylation of SLP-76, PRAM-1 and SKAP-HOM, down-regulating calcium signaling and production of anti-inflammatory IL-10, while extrusion of microbicidal neutrophil DNA (NETosis) is inhibited in a T3SS-dependent manner. In macrophages, specific YopM isoforms utilize an internal motif (YLTD) within the protein to directly sequester caspase-1 while other YopM isoforms target caspase-1 via the host scaffolding protein IQGAP1. (b) Triggering of host responses by the type III secretion system. Toll-like receptor 4 detection of the needle protein YscF activates NF-κB, inducing expression and production of pro-inflammatory cytokines. In contrast, inhibition of NF-κB and MAP kinase pathways by YopJ drives RIP kinase- and caspase-8-dependent activation of inflammatory caspase-1. Activation of caspase-1 also occurs upon translocation of YopB and YopD into the host cell cytosol. Additionally, sensing of YopE GTPase-activating protein activity can trigger killing of phagosomal Yersinia.

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