Role of macrophage apoptosis in the pathogenesis of Yersinia.
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.
Zhang
Y
Y
Department of Molecular Genetics and Microbiology, Center for Infectious Diseases, SUNY Stony Brook, Stony Brook, NY 11794-5222, USA.
Bliska
J B
JB
D017209:Apoptosis / Q000502:physiology*; D006801:Humans; D007410:Intestinal Diseases / Q000382:microbiology / Q000473:pathology*; D008264:Macrophages / Q000382:microbiology* / Q000473:pathology*; D015007:Yersinia / Q000472:pathogenicity*; D015009:Yersinia Infections / Q000382:microbiology / Q000473:pathology*