Modulation of Host Cell Death Pathways by Yersinia Species and the Type III Effector YopK

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Abstract

Pneumonic plague, caused by Yersinia pestis, is characterized by bacterial evasion and manipulation of the mammalian innate immune system. Following an initial anti-inflammatory response to infection in the lung, bacteria grow rapidly accompanied by host cell death and a massive inflammatory response. Phagocytic cells, in particular macrophages, are targeted and eliminated by the bacterial type III secretion system. In this work, we discuss the mechanisms by which the type III secretion system regulates host cell death during pulmonary infection by Y. pestis. We focus on the role of effector Yops E, J and K in this process and how they coordinately regulate cell death mechanisms that lead to precise control over inflammation during infection.