{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T05:39:02Z","timestamp":1790919542332,"version":"4.1.0"},"reference-count":56,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2004,8,1]],"date-time":"2004-08-01T00:00:00Z","timestamp":1091318400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2004,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Nitric oxide (NO) derived from inducible NO synthase (iNOS) contributes to the pathophysiology of acute lung injury (ALI). The effect of iNOS on pulmonary neutrophil infiltration in ALI is not known. Thus, we assessed pulmonary microvascular neutrophil sequestration through intravital videomicroscopy and pulmonary neutrophil infiltration, reflected by myeloperoxidase activity and lavage neutrophil counts, after induction of sepsis by cecal ligation\/perforation in wild-type (iNOS+\/+) versus iNOS\u2212\/\u2212 mice. Pulmonary microvascular neutrophil sequestration was attenuated in septic iNOS\u2212\/\u2212 versus iNOS+\/+ mice (15 \u00b1 1 vs. 20 \u00b1 1 leukocytes per field, p &amp;lt; 0.05), but lavage neutrophil counts were greater in iNOS\u2212\/\u2212 mice (5.7 \u00b1 1.5% vs. 0.7 \u00b1 0.1%, p &amp;lt; 0.05) between 6 and 18 hours after cecal ligation and perforation. When iNOS+\/+ bone marrow was transplanted into bone marrow\u2013depleted iNOS\u2212\/\u2212 mice (+ to \u2212 chimeras; iNOS limited to marrow-derived inflammatory cells), septic pulmonary microvascular neutrophil sequestration and lavage neutrophil counts were restored to levels seen in septic iNOS+\/+ mice. In contrast, in \u2212 to + chimeras, pulmonary neutrophil trafficking was similar to iNOS\u2212\/\u2212 mice. In vitro cytokine-stimulated neutrophil transendothelial migration was significantly greater for iNOS\u2212\/\u2212 versus iNOS+\/+ neutrophils (7.9 \u00b1 0.7% vs. 3.8 \u00b1 0.6%, p &amp;lt; 0.05) but was independent of endothelial iNOS. Thus, neutrophil iNOS-derived NO is an important autocrine modulator of pulmonary neutrophil infiltration in murine sepsis.<\/jats:p>","DOI":"10.1164\/rccm.200306-846oc","type":"journal-article","created":{"date-parts":[[2004,4,5]],"date-time":"2004-04-05T20:43:40Z","timestamp":1081197820000},"page":"227-233","source":"Crossref","is-referenced-by-count":134,"title":["Pulmonary Neutrophil Infiltration in Murine Sepsis"],"prefix":"10.1093","volume":"170","author":[{"given":"Habib M.","family":"Razavi","sequence":"first","affiliation":[{"name":"Vascular Biology Group, Lawson Health Research Institute, Division of Respirology, Departments of Medicine, Physiology, and Pharmacology, London Health Sciences Center, University of Western Ontario, London, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Le Feng","family":"Wang","sequence":"additional","affiliation":[{"name":"Vascular Biology Group, Lawson Health Research Institute, Division of Respirology, Departments of Medicine, Physiology, and Pharmacology, London Health Sciences Center, University of Western Ontario, London, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sean","family":"Weicker","sequence":"additional","affiliation":[{"name":"Vascular Biology Group, Lawson Health Research Institute, Division of Respirology, Departments of Medicine, Physiology, and Pharmacology, London Health Sciences Center, University of Western Ontario, London, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marta","family":"Rohan","sequence":"additional","affiliation":[{"name":"Vascular Biology Group, Lawson Health Research Institute, Division of Respirology, Departments of Medicine, Physiology, and Pharmacology, London Health Sciences Center, University of Western Ontario, London, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cedrin","family":"Law","sequence":"additional","affiliation":[{"name":"Vascular Biology Group, Lawson Health Research Institute, Division of Respirology, Departments of Medicine, Physiology, and Pharmacology, London Health Sciences Center, University of Western Ontario, London, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David G.","family":"McCormack","sequence":"additional","affiliation":[{"name":"Vascular Biology Group, Lawson Health Research Institute, Division of Respirology, Departments of Medicine, Physiology, and Pharmacology, London Health Sciences Center, University of Western Ontario, London, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sanjay","family":"Mehta","sequence":"additional","affiliation":[{"name":"Vascular Biology Group, Lawson Health Research Institute, Division of Respirology, Departments of Medicine, Physiology, and 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