AUTHOR=Yang Kun , He Yingxia , Park Chae Gyu , Kang Young Sun , Zhang Pei , Han Yanping , Cui Yujun , Bulgheresi Silvia , Anisimov Andrey P. , Dentovskaya Svetlana V. , Ying Xiaoling , Jiang Lingyu , Ding Honghui , Njiri Olivia Adhiambo , Zhang Shusheng , Zheng Guoxing , Xia Lianxu , Kan Biao , Wang Xin , Jing Huaiqi , Yan Meiying , Li Wei , Wang Yuanzhi , Xiamu Xiding , Chen Gang , Ma Ding , Bartra Sara Schesser , Plano Gregory V. , Klena John D. , Yang Ruifu , Skurnik Mikael , Chen Tie TITLE=Yersinia pestis Interacts With SIGNR1 (CD209b) for Promoting Host Dissemination and Infection JOURNAL=Frontiers in Immunology VOLUME=10 YEAR=2019 URL=https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2019.00096 DOI=10.3389/fimmu.2019.00096 ISSN=1664-3224 ABSTRACT=

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.