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1 Medicine and Immunology, Roswell Park Cancer Institute, Buffalo, New York, United States
2 Anesthesiology, University at Buffalo-SUNY, 247 BRB, Buffalo, New York, 14214, United States; Pathology, University at Buffalo-SUNY, Buffalo, New York, United States
3 Biostatistics, University at Buffalo-SUNY, Buffalo, New York, United States
4 Medicine, University at Buffalo-SUNY, Buffalo, New York, United States
5 Pediatrics, University at Buffalo-SUNY, Buffalo, New York, United States; Gynecology-Obstetrics, University at Buffalo-SUNY, Buffalo, New York, United States; Pharmacology, University at Buffalo-SUNY, Buffalo, New York, United States
6 Anesthesiology, University at Buffalo-SUNY, Buffalo, New York, United States
7 Laboratory of Clinical Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States
8 Anesthesiology, University at Buffalo-SUNY, Buffalo, New York, United States; Microbiology, University at Buffalo-SUNY, Buffalo, New York, United States
* To whom correspondence should be addressed. E-mail: prknight{at}buffalo.edu.
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 p47phox-/- knockout mouse model of chronic granulomatous disease (CGD) was used. p47phox-/- mice developed a significantly greater alveolar neutrophilic leukocytosis compared to wild type mice at all time points after acid injury, with the difference between genotypes being most marked at 48 hr. In contrast, the p47phox-/- mice had a decreased number of macrophages in bronchoalveloar lavage (BAL) compared to wild types at 48 hr after acid or saline aspiration. Albumin concentration in BAL reflecting capillary leak was also greater in p47phox-/- compared to wild type mice. BAL concentrations of pro-inflammatory cytokines and chemokines were greater in p47phox-/- compared to 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 down modulating 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.
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