{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,11]],"date-time":"2026-02-11T13:25:46Z","timestamp":1770816346388,"version":"3.50.1"},"reference-count":63,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2021,4,1]],"date-time":"2021-04-01T00:00:00Z","timestamp":1617235200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":["www.atsjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2021,4,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Streptococcus pneumoniae is the leading cause of hospital community-acquired pneumonia. Patients with pneumococcal pneumonia may develop complicated parapneumonic effusions or empyema that can lead to pleural organization and subsequent fibrosis. The pathogenesis of pleural organization and scarification involves complex interactions between the components of the immune system, coagulation, and fibrinolysis. EPCR (endothelial protein C receptor) is a critical component of the protein C anticoagulant pathway. The present study was performed to evaluate the role of EPCR in the pathogenesis of S. pneumoniae infection\u2013induced pleural thickening and fibrosis. Our studies show that the pleural mesothelium expresses EPCR. Intrapleural instillation of S. pneumoniae impairs lung compliance and lung volume in wild-type and EPCR-overexpressing mice but not in EPCR-deficient mice. Intrapleural S. pneumoniae infection induces pleural thickening in wild-type mice. Pleural thickening is more pronounced in EPCR-overexpressing mice, whereas it is reduced in EPCR-deficient mice. Markers of mesomesenchymal transition are increased in the visceral pleura of S. pneumoniae\u2013infected wild-type and EPCR-overexpressing mice but not in EPCR-deficient mice. The lungs of wild-type and EPCR-overexpressing mice administered intrapleural S. pneumoniae showed increased infiltration of macrophages and neutrophils, which was significantly reduced in EPCR-deficient mice. An analysis of bacterial burden in the pleural lavage, the lungs, and blood revealed a significantly lower bacterial burden in EPCR-deficient mice compared with wild-type and EPCR-overexpressing mice. Overall, our data provide strong evidence that EPCR deficiency protects against S. pneumoniae infection\u2013induced impairment of lung function and pleural remodeling.<\/jats:p>","DOI":"10.1165\/rcmb.2020-0328oc","type":"journal-article","created":{"date-parts":[[2021,2,18]],"date-time":"2021-02-18T18:39:43Z","timestamp":1613673583000},"page":"477-491","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":14,"title":["Endothelial Cell Protein C Receptor Deficiency Attenuates\n                    <i>Streptococcus pneumoniae\u2013<\/i>\n                    Induced Pleural Fibrosis"],"prefix":"10.1093","volume":"64","author":[{"given":"Shiva","family":"Keshava","sequence":"first","affiliation":[{"name":"Department of Cellular and Molecular Biology"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jhansi","family":"Magisetty","sequence":"additional","affiliation":[{"name":"Department of Cellular and Molecular Biology"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Torry A.","family":"Tucker","sequence":"additional","affiliation":[{"name":"Department of Cellular and Molecular Biology"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Weshely","family":"Kujur","sequence":"additional","affiliation":[{"name":"Department of Pulmonary Immunology, The University of Texas Health Science Center at Tyler, Tyler, Texas; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sachin","family":"Mulik","sequence":"additional","affiliation":[{"name":"Department of Pulmonary Immunology, The University of Texas Health Science Center at Tyler, Tyler, Texas; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Charles T.","family":"Esmon","sequence":"additional","affiliation":[{"name":"Coagulation Biology Laboratory, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Steven","family":"Idell","sequence":"additional","affiliation":[{"name":"Department of Cellular and Molecular Biology"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L. 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