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Fibrin facilitates both innate and T cell-mediated defense against Yersinia pestis
Deyan Luo1, Jr-Shiuan Lin, Michelle A Parent
1Trudeau Institute, Saranac Lake, NY 12983, USA.
Abstract:
The Gram-negative bacterium Yersinia pestis causes plague, a rapidly progressing and often fatal disease. The formation of fibrin at sites of Y. pestis infection supports innate host defense against plague, perhaps by providing a nondiffusible spatial cue that promotes the accumulation of inflammatory cells expressing fibrin-binding integrins. This report demonstrates that fibrin is an essential component of T cell-mediated defense against plague but can be dispensable for Ab-mediated defense. Genetic or pharmacologic depletion of fibrin abrogated innate and T cell-mediated defense in mice challenged intranasally with Y. pestis. The fibrin-deficient mice displayed reduced survival, increased bacterial burden, and exacerbated hemorrhagic pathology. They also showed fewer neutrophils within infected lung tissue and reduced neutrophil viability at sites of liver infection. Depletion of neutrophils from wild-type mice weakened T cell-mediated defense against plague. The data suggest that T cells combat plague in conjunction with neutrophils, which require help from fibrin to withstand Y. pestis encounters and effectively clear bacteria.
Insights
Fibrin is crucial for T cell-mediated defense against Yersinia pestis (plague). Without fibrin, mice showed reduced survival and increased bacterial load, highlighting fibrin
Area of Science:
- Immunology
- Microbiology
- Pathology
Background:
- Yersinia pestis causes plague, a severe bacterial infection.
- Fibrin formation at infection sites may aid innate immunity by attracting immune cells.
- The role of fibrin in adaptive immunity against Y. pestis is not fully understood.
Purpose of the Study:
- To investigate the essentiality of fibrin in host defense against Yersinia pestis.
- To determine fibrin's role in T cell-mediated versus antibody-mediated immunity.
- To elucidate the contribution of fibrin to neutrophil function during plague.
Main Methods:
- Genetic or pharmacologic depletion of fibrin in a mouse model of intranasal Y. pestis infection.
- Assessment of survival, bacterial burden, and hemorrhagic pathology.
- Analysis of neutrophil infiltration, viability, and T cell-mediated immunity.
Main Results:
- Fibrin depletion abrogated innate and T cell-mediated defense against Y. pestis.
- Fibrin-deficient mice exhibited decreased survival, higher bacterial load, and worsened pathology.
- Fibrin is essential for T cell-mediated defense but dispensable for antibody-mediated defense.
Conclusions:
- Fibrin is a critical component of T cell-driven immunity against Yersinia pestis.
- Fibrin supports neutrophil function, enhancing bacterial clearance and host survival.
- T cells and neutrophils collaborate to combat plague, with fibrin facilitating this interaction.
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