{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T16:16:11Z","timestamp":1790612171207,"version":"4.1.0"},"reference-count":24,"publisher":"Wiley","issue":"13","license":[{"start":{"date-parts":[[2024,7,9]],"date-time":"2024-07-09T00:00:00Z","timestamp":1720483200000},"content-version":"vor","delay-in-days":8,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Physiological Reports"],"published-print":{"date-parts":[[2024,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Endothelial dysfunction is a critical feature of acute respiratory distress syndrome (ARDS) associated with higher disease severity and worse outcomes. Preclinical in\u00a0vivo models of sepsis and ARDS have failed to yield useful therapies in humans, perhaps due to interspecies differences in inflammatory responses and heterogeneity of human host responses. Use of microphysiological systems (MPS) to investigate lung endothelial function may shed light on underlying mechanisms and targeted treatments for ARDS. We assessed the response to plasma from critically ill sepsis patients in our lung endothelial MPS through measurement of endothelial permeability, expression of adhesion molecules, and inflammatory cytokine secretion. Sepsis plasma induced areas of endothelial cell (EC) contraction, loss of cellular coverage, and luminal defects. EC barrier function was significantly worse following incubation with sepsis plasma compared to healthy plasma. EC ICAM\u20101 expression, IL\u20106 and soluble ICAM\u20101 secretion increased significantly more after incubation with sepsis plasma compared with healthy plasma. Plasma from sepsis patients who developed ARDS further increased IL\u20106 and sICAM\u20101 compared to plasma from sepsis patients without ARDS and healthy plasma. Our results demonstrate the proof of concept that lung endothelial MPS can enable interrogation of specific mechanisms of endothelial dysfunction that promote ARDS in sepsis patients.<\/jats:p>","DOI":"10.14814\/phy2.16134","type":"journal-article","created":{"date-parts":[[2024,7,10]],"date-time":"2024-07-10T01:55:37Z","timestamp":1720576537000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Modeling lung endothelial dysfunction in sepsis\u2010associated <scp>ARDS<\/scp> using a microphysiological system"],"prefix":"10.14814","volume":"12","author":[{"given":"Nai\u2010Wen","family":"Liang","sequence":"first","affiliation":[{"name":"Department of Biomedical Engineering University of Wisconsin  Madison Wisconsin USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carole","family":"Wilson","sequence":"additional","affiliation":[{"name":"Division of Allergy, Pulmonary and Critical Care, Department of Medicine, School of Medicine and Public Health University of Wisconsin  Madison Wisconsin USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brooke","family":"Davis","sequence":"additional","affiliation":[{"name":"College of Letters and Science University of Wisconsin  Madison Wisconsin USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ian","family":"Wolf","sequence":"additional","affiliation":[{"name":"Department of anesthesiology and Perioperative Care University of California Irvine  Irvine USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tonela","family":"Qyli","sequence":"additional","affiliation":[{"name":"Department of Medicine, School of Medicine and Public Health University of Wisconsin  Madison Wisconsin USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joy","family":"Moy","sequence":"additional","affiliation":[{"name":"Division of Allergy, Pulmonary and Critical Care, Department of Medicine, School 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