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Yersinia pestis Interacts With SIGNR1 (CD209b) for Promoting Host Dissemination and Infection
Kun Yang1,2, Yingxia He1, Chae Gyu Park3
1Department of Clinical Immunology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Frontiers in Immunology
|March 28, 2019
Summary
Yersinia pestis uses its core lipopolysaccharide (LPS) to bind to antigen-presenting cells (APCs), promoting plague dissemination. This LPS interaction is key to Yersinia pseudotuberculosis evolving into the highly virulent Yersinia pestis.
Area of Science:
- Microbiology
- Immunology
- Evolutionary Biology
Background:
- Yersinia pestis causes plague, evolving from Yersinia pseudotuberculosis.
- Mechanisms of Y. pestis virulence evolution remain unclear.
- Y. pestis lacks the O-antigen found in Y. pseudotuberculosis LPS.
Purpose of the Study:
- Investigate how Y. pestis evolved increased virulence.
- Determine the role of LPS in Y. pestis pathogenesis.
- Elucidate the interaction between Y. pestis and host immune cells.
Main Methods:
- Comparative analysis of Yersinia LPS structures.
- In vitro studies of Y. pestis interaction with antigen-presenting cells (APCs).
- In vivo assessment of bacterial dissemination.
Main Results:
- Y. pestis core LPS binds to the SIGNR1 receptor on APCs.
- This interaction facilitates bacterial spread to lymph nodes, spleen, and liver.
- Loss of O-antigen is critical for APC hijacking and systemic infection.
Conclusions:
- Y. pestis's core LPS interaction with SIGNR1 is a key virulence mechanism.
- O-antigen loss is a critical evolutionary step enabling Y. pestis pathogenesis.
- This mechanism explains Y. pestis's enhanced dissemination and systemic infection capability.
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