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Updated: Jun 25, 2026
Depletion and Reconstitution of Macrophages in Mice
Published on: August 1, 2012
Yersinia pestis and host macrophages: immunodeficiency of mouse macrophages induced by YscW
Yujing Bi1, Zongmin Du, Yanping Han
1State Key laboratory of Pathogen and Biosecurity, National Center for Biomedical Analysis, Army Center for Microbial Detection and Research, Institute of Microbiology and Epidemiology, Beijing, China.
Abstract:
The virulence of the pathogenic Yersinia species depends on a plasmid-encoded type III secretion system (T3SS) that transfers six Yersinia outer protein (Yop) effector proteins into the cytoplasm of eukaryotic cells, leading to disruption of host defence mechanisms. It is shown in this study that Yersinia pestis YscW, a protein of the T3SS injectisome, contributes to the induction of a deficiency in phagocytosis in host macrophages and a reduction in their antigen-presenting capacity. A Y. pestis strain lacking yscW had no effect on uptake by host macrophages. In mice infected with wild-type Y. pestis, the yscW mutant or a complement strain, immunodeficiency was observed in host macrophages compared with those from uninfected mice. However, the phagocytosis and antigen presenting capacities of macrophages infected by yscW mutant strain both in vivo and in vitro were significantly higher than those by wild type strain. Consistent with this finding, when YscW was expressed in the RAW264.7 macrophage cell line, phagocytosis and antigen-presenting capacities were significantly lower than those of the control groups. These results indicate that Y. pestis YscW may directly induce immunodeficiency in murine macrophages by crippling their phagocytosis and antigen-presenting capacities. These data provide evidences to Y. pestis pathogenesis that some proteins in T3SS injectisome, such as YscW protein, might play independent roles in disrupting host defense apart from their known functions.
Insights
Yersinia pestis YscW protein disrupts host immunity by impairing macrophage phagocytosis and antigen presentation. This study reveals YscW
Area of Science:
- Microbiology
- Immunology
- Pathogenesis
Background:
- Pathogenic Yersinia species utilize a type III secretion system (T3SS) to deliver Yersinia outer proteins (Yops) into host cells, suppressing immune responses.
- The T3SS injectisome is crucial for virulence, but individual component roles in host immune disruption are not fully elucidated.
Purpose of the Study:
- To investigate the specific role of Yersinia pestis YscW, a T3SS injectisome protein, in modulating host macrophage functions.
- To determine if YscW contributes independently to Yersinia pathogenesis by affecting phagocytosis and antigen presentation.
Main Methods:
- Comparative analysis of Yersinia pestis wild-type, yscW mutant, and complemented strains in murine infection models.
- In vitro assessment of macrophage phagocytosis and antigen-presenting capacity upon infection with different Y. pestis strains.
- Experimental expression of YscW in RAW264.7 macrophage cell line to evaluate its direct impact on cellular functions.
Main Results:
- Mice infected with wild-type Y. pestis exhibited immunodeficiency in macrophages, while the yscW mutant showed less impact.
- Macrophages infected with the yscW mutant displayed significantly higher phagocytosis and antigen-presenting capacities compared to wild-type infections, both in vivo and in vitro.
- Expression of YscW in RAW264.7 cells led to a significant decrease in phagocytosis and antigen presentation.
Conclusions:
- Yersinia pestis YscW directly induces immunodeficiency in murine macrophages by compromising their phagocytic and antigen-presenting capabilities.
- YscW plays an independent role in Yersinia pathogenesis, contributing to host defense disruption beyond its established function within the T3SS injectisome.
