{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,14]],"date-time":"2026-02-14T05:48:05Z","timestamp":1771048085108,"version":"3.50.1"},"reference-count":29,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Lung Cellular and Molecular Physiology"],"published-print":{"date-parts":[[2012,1,1]]},"abstract":"<jats:p> The antioxidant enzyme extracellular superoxide dismutase (EC-SOD) is abundant in the lung and is known to limit inflammation and fibrosis following numerous pulmonary insults. Previous studies have reported a loss of full-length EC-SOD from the pulmonary parenchyma with accumulation of proteolyzed EC-SOD in the airspace after an interstitial lung injury. However, following airspace only inflammation, EC-SOD accumulates in the airspace without a loss from the interstitium, suggesting this antioxidant may be released from an extrapulmonary source. Because leukocytes are known to express EC-SOD and are prevalent in the bronchoalveolar lavage fluid (BALF) after injury, it was hypothesized that these cells may transport and release EC-SOD into airspaces. To test this hypothesis, C57BL\/6 wild-type and EC-SOD knockout mice were irradiated and transplanted with bone marrow from either wild-type mice or EC-SOD knockout mice. Bone marrow chimeric mice were then intratracheally treated with asbestos and killed 3 and 7 days later. At both 3 and 7 days following asbestos injury, mice without pulmonary EC-SOD expression but with EC-SOD in infiltrating and resident leukocytes did not have detectable levels of EC-SOD in the airspaces. In addition, leukocyte-derived EC-SOD did not significantly lessen inflammation or early stage fibrosis that resulted from asbestos injury in the lungs. Although it is not influential in the asbestos-induced interstitial lung injury model, EC-SOD is still known to be present in leukocytes and may play an influential role in attenuating pneumonias and other inflammatory diseases. <\/jats:p>","DOI":"10.1152\/ajplung.00360.2010","type":"journal-article","created":{"date-parts":[[2011,10,15]],"date-time":"2011-10-15T02:43:03Z","timestamp":1318646583000},"page":"L160-L166","source":"Crossref","is-referenced-by-count":5,"title":["Leukocyte-derived extracellular superoxide dismutase does not contribute to airspace EC-SOD after interstitial pulmonary injury"],"prefix":"10.1152","volume":"302","author":[{"given":"Michelle L.","family":"Manni","sequence":"first","affiliation":[{"name":"Departments of 1Pathology,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael W.","family":"Epperly","sequence":"additional","affiliation":[{"name":"Radiation Oncology,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wei","family":"Han","sequence":"additional","affiliation":[{"name":"Division of Allergy, Department of Medicine, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Timothy S.","family":"Blackwell","sequence":"additional","affiliation":[{"name":"Division of Allergy, Department of Medicine, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Steven R.","family":"Duncan","sequence":"additional","affiliation":[{"name":"Medicine, and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jon D.","family":"Piganelli","sequence":"additional","affiliation":[{"name":"Pediatrics, University of Pittsburgh, Pittsburgh, Pennsylvania; 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