Yersinia pestis Interacts With SIGNR1 (CD209b) for Promoting Host Dissemination and Infection
oleh: Kun Yang, Kun Yang, Yingxia He, Chae Gyu Park, Young Sun Kang, Pei Zhang, Yanping Han, Yujun Cui, Silvia Bulgheresi, Andrey P. Anisimov, Svetlana V. Dentovskaya, Xiaoling Ying, Lingyu Jiang, Honghui Ding, Olivia Adhiambo Njiri, Olivia Adhiambo Njiri, Shusheng Zhang, Guoxing Zheng, Lianxu Xia, Biao Kan, Xin Wang, Huaiqi Jing, Meiying Yan, Wei Li, Yuanzhi Wang, Xiding Xiamu, Gang Chen, Ding Ma, Sara Schesser Bartra, Gregory V. Plano, John D. Klena, Ruifu Yang, Mikael Skurnik, Tie Chen, Tie Chen
| Format: | Article |
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| Diterbitkan: | Frontiers Media S.A. 2019-03-01 |
Deskripsi
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.