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Yersinia pestis , a Gram-negative bacterium and the etiologic agent of plague, has evolved from  Yersinia pseudotuberculosis , a cause of a mild enteric disease. However, the molecular and biological mechanisms of how  Y. pseudotuberculosis  evolved to such a remarkably virulent pathogen,  Y. pestis , are not clear. The ability to initiate a rapid bacterial dissemination is a characteristic hallmark of  Y. pestis  infection. A distinguishing characteristic between the two  Yersinia  species is that  Y. pseudotuberculosis  strains possess an O-antigen of lipopolysaccharide (LPS) while  Y. pestis  has lost the O-antigen during evolution and therefore exposes its core LPS. In this study, we showed that  Y. pestis  utilizes its core LPS to interact with SIGNR1 (CD209b), a C-type lectin receptor on antigen presenting cells (APCs), leading to bacterial dissemination to lymph nodes, spleen and liver, and the initiation of a systemic infection. We therefore propose that the loss of O-antigen represents a critical step in the evolution of  Y. pseudotuberculosis  into  Y. pestis  in terms of hijacking APCs, promoting bacterial dissemination and causing the plague.

Yersinia pestis Interacts With SIGNR1 (CD209b) for Promoting Host Dissemination and Infection