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Many pathogens usurp the host hemostatic system during infection to promote pathogenesis.Yersinia pestis , the causative agent of plague, expresses the plasminogen activator protease Pla, which has been shownin vitro to target and cleave multiple proteins within the fibrinolytic pathway, including the plasmin inhibitor α2-antiplasmin (A2AP). It is not known, however, if Pla inactivates A2APin vivo ; the role of A2AP during respiratoryY. pestis infection is not known either. Here, we show thatY. pestis does not appreciably cleave A2AP in a Pla-dependent manner in the lungs during experimental pneumonic plague. Furthermore, following intranasal infection withY. pestis , A2AP-deficient mice exhibit no difference in survival time, bacterial burden in the lungs, or dissemination from wild-type mice. Instead, we found that in the absence of Pla, A2AP contributes to the control of the pulmonary inflammatory response during infection by reducing neutrophil recruitment and cytokine production, resulting in altered immunopathology of the lungs compared to A2AP-deficient mice. Thus, our data demonstrate that A2AP is not significantly affected by the Pla protease during pneumonic plague, and although A2AP participates in immune modulation in the lungs, it has limited impact on the course or ultimate outcome of the infection.

Impact of the Pla Protease Substrate α2-Antiplasmin on the Progression of Primary Pneumonic Plague