{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T05:01:31Z","timestamp":1761541291184,"version":"3.40.5"},"reference-count":51,"publisher":"American Society for Microbiology","issue":"12","license":[{"start":{"date-parts":[[2015,12,1]],"date-time":"2015-12-01T00:00:00Z","timestamp":1448928000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2015,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Many pathogens usurp the host hemostatic system during infection to promote pathogenesis.\n            <jats:named-content content-type=\"genus-species\">Yersinia pestis<\/jats:named-content>\n            , the causative agent of plague, expresses the plasminogen activator protease Pla, which has been shown\n            <jats:italic>in vitro<\/jats:italic>\n            to target and cleave multiple proteins within the fibrinolytic pathway, including the plasmin inhibitor \u03b12-antiplasmin (A2AP). It is not known, however, if Pla inactivates A2AP\n            <jats:italic>in vivo<\/jats:italic>\n            ; the role of A2AP during respiratory\n            <jats:named-content content-type=\"genus-species\">Y. pestis<\/jats:named-content>\n            infection is not known either. Here, we show that\n            <jats:named-content content-type=\"genus-species\">Y. pestis<\/jats:named-content>\n            does not appreciably cleave A2AP in a Pla-dependent manner in the lungs during experimental pneumonic plague. Furthermore, following intranasal infection with\n            <jats:named-content content-type=\"genus-species\">Y. pestis<\/jats:named-content>\n            , 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.\n          <\/jats:p>","DOI":"10.1128\/iai.01086-15","type":"journal-article","created":{"date-parts":[[2015,10,6]],"date-time":"2015-10-06T00:11:36Z","timestamp":1444090296000},"page":"4837-4847","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":20,"title":["Impact of the Pla Protease Substrate \u03b12-Antiplasmin on the Progression of Primary Pneumonic Plague"],"prefix":"10.1128","volume":"83","author":[{"given":"Justin L.","family":"Eddy","sequence":"first","affiliation":[{"name":"Department of Microbiology-Immunology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jay 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