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This Article Full Text Full Text (PDF) All Versions of this Article: 292/3/L760    most recent 00281.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Segal, B. H. Articles by Knight, P. R. Search for Related Content PubMed PubMed Citation Articles by Segal, B. H. Articles by Knight, P. R., III

Acid aspiration-induced lung inflammation and injury are exacerbated in NADPH oxidase-deficient mice

¹Departments of Medicine and Immunology, Roswell Park Cancer Institute, ²Departments of Anesthesiology and Pathology, School of Medicine, ³Department of Biostatistics, School of Public Health and Health Professions, ⁴Department of Medicine, School of Medicine, ⁵Departments of Pediatrics, Gynecology-Obstetrics, and Pharmacology, School of Medicine, and ⁶Department of Anesthesiology, School of Medicine, University at Buffalo-State University of New York, Buffalo, New York; ⁷Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland; and ⁸Departments of Anesthesiology and Microbiology, School of Medicine, University at Buffalo-State University of New York, Buffalo, New York

Submitted 26 July 2006 ; accepted in final form 10 November 2006

Increased reactive oxidant intermediates (ROIs) from primed leukocytes have been implicated in the pathogenesis of acid aspiration lung injury. To evaluate the specific role of the phagocyte NADPH oxidase-derived ROIs in acid lung injury, the p47^phox–/– knockout mouse model of chronic granulomatous disease was used. p47^phox–/– mice developed a significantly greater alveolar neutrophilic leukocytosis compared with wild-type mice at all time points after acid injury, with the difference between genotypes being most marked at 48 h. In contrast, the p47^phox–/– mice had a decreased number of macrophages in bronchoalveolar lavage (BAL) compared with wild-type at 48 h after acid or saline aspiration. Albumin concentration in BAL reflecting capillary leak was also greater in p47^phox–/– compared with wild-type mice. BAL concentrations of proinflammatory cytokines and chemokines were greater in p47^phox–/– compared with wild-type mice. These findings suggest that NADPH oxidase, directly or indirectly, plays a role in attenuating the acute neutrophilic response after acid lung injury. We speculate that this downmodulating effect may be mediated by promoting the transition from production of cytokines and chemokines involved in neutrophilic infiltration to a less injurious, chronic inflammatory response.

acid aspiration pneumonitis; chronic granulomatous disease; reactive oxidants; acute respiratory distress syndrome

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