Yersinia pestis interacts with SIGNR1 (CD209b) for promoting host dissemination and infection

K. Yang; Y. He; C. Park; Y. Kang; P. Zhang; Y. Han; Y. Cui; S. Bulgheresi; A. Anisimov; S. Dentovskaya; X. Ying; L. Jiang; H. Ding; O. Njiri; S. Zhang; G. Zheng; L. Xia; B. Kan; X. Wang; H. Jing; M. Yan; W. Li; Y. Wang; X. Xiamu; G. Chen; D. Ma; S. Bartra; G. Plano; J. Klena; R. Yang; M. Skurnik; T. Chen

Статья

Yersinia pestis interacts with SIGNR1 (CD209b) for promoting host dissemination and infection

K. Yang, Y. He, C. Park, Y. Kang, P. Zhang, Y. Han, Y. Cui, S. Bulgheresi, A. Anisimov, S. Dentovskaya, X. Ying, L. Jiang, H. Ding, O. Njiri, S. Zhang, G. Zheng, L. Xia, B. Kan, X. Wang, H. Jing, M. Yan, W. Li, Y. Wang, X. Xiamu, G. Chen, D. Ma, S. Bartra, G. Plano, J. Klena, R. Yang, M. Skurnik, T. Chen,

2021

https://doi.org/10.3389/fimmu.2019.00096

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. Copyright © 2019 Yang, He, Park, Kang, Zhang, Han, Cui, Bulgheresi, Anisimov, Dentovskaya, Ying, Jiang, Ding, Njiri, Zhang, Zheng, Xia, Kan, Wang, Jing, Yan, Li, Wang, Xiamu, Chen, Ma, Bartra, Plano, Klena, Yang, Skurnik and Chen.

Цитирование

Источник

Версии

1. Version of Record от 2021-04-27

Метаданные

Об авторах

K. Yang
Department of Clinical Immunology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
Y. He
Department of Pathogen Biology and Immunology, Shihezi University School of Medicine, Shihezi, China
C. Park
Laboratory of Immunology, Brain Korea 21 PLUS Project for Medical Science, Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, South Korea
Y. Kang
Department of Biomedical Sciences, College of Medicine, University of Illinois at Chicago, Chicago, IL, United States
P. Zhang
State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, China
Y. Han
Department of Ecogenomics and Systems Biology, University of Vienna, Vienna, Austria
Y. Cui
State Research Center for Applied Microbiology and Biotechnology, Obolensk, Russian Federation
S. Bulgheresi
Department of Biological Sciences, Faculty of Science, Technology and Engineering, Chuka University, Chuka, Kenya
A. Anisimov
National Institute for Communicable Diseases Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing, China
S. Dentovskaya
Institute of Organ Transplantation, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
X. Ying
Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
L. Jiang
Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL, United States
H. Ding
School of Biological Sciences, University of Canterbury, Christchurch, New Zealand
O. Njiri
Department of Bacteriology and Immunology, Haartman Institute, Helsinki University Central Hospital Laboratory Diagnostics, University of Helsinki, Helsinki, Finland
S. Zhang
G. Zheng
L. Xia
B. Kan
X. Wang
H. Jing
M. Yan
W. Li
Y. Wang
X. Xiamu
G. Chen
D. Ma
S. Bartra
G. Plano
J. Klena
R. Yang
M. Skurnik
T. Chen

Название журнала

Frontiers in Immunology

Том

Выпуск

Страницы

Ключевые слова

carcinoembryonic antigen related cell adhesion molecule 1; carcinoembryonic antigen related cell adhesion molecule 6; complementary DNA; lipopolysaccharide; O antigen; cell adhesion molecule; cell surface receptor; DC-specific ICAM-3 grabbing nonintegrin; lectin; animal experiment; animal model; antigen presenting cell; Article; bacterial strain; bioluminescence; cell isolation; controlled study; Escherichia coli; female; flow cytometry; gene deletion; gene sequence; H1HeLa cell line; male; mouse; nonhuman; peritoneum macrophage; phagocytosis; plague; plasmid; serotype; Shigella dysenteriae; Yersinia pestis; Yersinia pseudotuberculosis; animal; Bagg albino mouse; C57BL mouse; cell line; genetics; HeLa cell line; host pathogen interaction; human; immunology; knockout mouse; macrophage; physiology; plague; Yersinia pestis; Yersinia pseudotuberculosis infection; Animals; Antigen-Presenting Cells; Cell Adhesion Molecules; Cell Line; Female; HeLa Cells; Host-Pathogen Interactions; Humans; Lectins, C-Type; Lipopolysaccharides; Macrophages; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Knockout; Plague; Receptors, Cell Surface; Yersinia pestis; Yersinia pseudotuberculosis; Yersinia pseudotuberculosis Infections

Издатель

Frontiers Media S.A.

Тип документа

journal article

Тип лицензии Creative Commons

Правовой статус документа

Свободная лицензия

Источник

scopus

Поиск по репозиторию

Статья

Yersinia pestis interacts with SIGNR1 (CD209b) for promoting host dissemination and infection

Похожие публикации

Источник

Версии

Метаданные