38 48

Cited 0 times in

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

Authors
 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  ;  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 
Citation
 FRONTIERS IN IMMUNOLOGY, Vol.10 : 96, 2019 
Journal Title
 FRONTIERS IN IMMUNOLOGY 
Issue Date
2019
Keywords
SIGNR1 (CD209b) ; Yersinia pestis ; antigen presenting cells (APCs) ; bacterial dissemination ; core lipopolysaccharide/lipooligosaccharides (core LPS/LOS) ; dendritic cells (DCs) ; host-pathogen interactions ; macrophages
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.
Files in This Item:
T201901511.pdf Download
DOI
10.3389/fimmu.2019.00096
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
Yonsei Authors
Park, Chae Gyu(박채규) ORCID logo https://orcid.org/0000-0003-1906-1308
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/169904
사서에게 알리기
  feedback

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse