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Here we show that two important human pathogens, the plague bacterium<jats:italic>Yersinia pestis<\/jats:italic>and the enteropathogen<jats:italic>Salmonella enterica<\/jats:italic>serovar Typhimurium, inactivate PAI-1 by cleaving the R346-M347 bait peptide bond in the reactive center loop. No cleavage of PAI-1 was detected with<jats:italic>Yersinia pseudotuberculosis<\/jats:italic>, an oral\/fecal pathogen from which<jats:italic>Y. pestis<\/jats:italic>has evolved, or with<jats:italic>Escherichia coli<\/jats:italic>. The cleavage and inactivation of PAI-1 were mediated by the outer membrane proteases plasminogen activator Pla of<jats:italic>Y. pestis<\/jats:italic>and PgtE protease of<jats:italic>S. enterica<\/jats:italic>, which belong to the omptin family of transmembrane endopeptidases identified in Gram-negative bacteria. Cleavage of PAI-1 was also detected with the omptins Epo of<jats:italic>Erwinia pyrifoliae<\/jats:italic>and Kop of<jats:italic>Klebsiella pneumoniae<\/jats:italic>, which both belong to the same omptin subfamily as Pla and PgtE, whereas no cleavage of PAI-1 was detected with omptins of<jats:italic>Shigella flexneri<\/jats:italic>or<jats:italic>E. coli<\/jats:italic>or the<jats:italic>Yersinia<\/jats:italic>chromosomal omptins, which belong to other omptin subfamilies. The results reveal a novel serpinolytic mechanism by which enterobacterial species expressing omptins of the Pla subfamily bypass normal control of host proteolysis.<\/jats:p>","DOI":"10.1128\/jb.00458-10","type":"journal-article","created":{"date-parts":[[2010,7,17]],"date-time":"2010-07-17T01:45:48Z","timestamp":1279331148000},"page":"4553-4561","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":48,"title":["The Omptins of<i>Yersinia pestis<\/i>and<i>Salmonella enterica<\/i>Cleave the Reactive Center Loop of Plasminogen Activator Inhibitor 1"],"prefix":"10.1128","volume":"192","author":[{"given":"Johanna","family":"Haiko","sequence":"first","affiliation":[{"name":"General Microbiology, Department of Biosciences, P.O. Box 56"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liisa","family":"Laakkonen","sequence":"additional","affiliation":[{"name":"General Microbiology, Department of Biosciences, P.O. Box 56"},{"name":"Neuroscience Center, P.O. Box 56"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katri","family":"Juuti","sequence":"additional","affiliation":[{"name":"General Microbiology, Department of Biosciences, P.O. Box 56"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nisse","family":"Kalkkinen","sequence":"additional","affiliation":[{"name":"Institute of Biotechnology, P.O. Box 65, University of Helsinki, FI 00014 Helsinki, Finland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Timo K.","family":"Korhonen","sequence":"additional","affiliation":[{"name":"General Microbiology, Department of Biosciences, P.O. Box 56"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","first-page":"14043","DOI":"10.1073\/pnas.96.24.14043","volume":"96","year":"1999","unstructured":"Achtman, M., K. Aurth, G. Morelli, G. Torrea, A. Guiyoule, and E. Carniel. 1999. 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