Frontiers in Immunology (Mar 2019)

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

  • 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

DOI
https://doi.org/10.3389/fimmu.2019.00096
Journal volume & issue
Vol. 10

Abstract

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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.

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