Role of Macrophage Apoptosis in the Pathogenesis of Yersinia

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Abstract
Yersinia species that are pathogenic for humans (Yersinia pestis, Yersinia pseudotuberculosis, and Yersinia enterocolitica) induce apoptosis in macrophages. Yersinia-induced apoptosis utilizes the mitochondrial pathway and is executed by activation of caspase cascades. The mechanism of Yersinia-induced apoptosis in macrophages has two essential components. One component is the innate immune response of macrophages to the pathogen, which leads to the activation of a survival response and a death response. Recognition of the bacterial cell envelope component lipopolysaccharide by Toll-like receptor 4 (TLR4) constitutes an important part of the innate immune response to the pathogen. The second essential component is YopJ, a protein secreted into Yersinia-infected macrophages via a bacterial type III secretion system, which selectively shuts down the survival pathway. In the absence of the survival pathway, the death pathway is executed, and Yersinia-infected macrophages undergo apoptosis. In this review, we introduce the basic features of Yersinia pathogenesis, summarize our current understanding of Yersinia-induced apoptosis, and discuss the role of apoptosis during Yersinia infection.