NDLI: NADPH oxidase and Nrf2 regulate gastric aspiration-induced inflammation and acute lung injury.

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NADPH oxidase and Nrf2 regulate gastric aspiration-induced inflammation and acute lung injury.

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NADPH oxidase and Nrf2 regulate gastric aspiration-induced inflammation and acute lung injury.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Grimm, Melissa J. Mullan, Barbara A. Sporn, Michael B. Blackwell, Timothy S. Knight, Paul R. Itagaki, Kiyoshi Hauser, Carl J. Davidson, Bruce A. Raghavendran, Krishnan Vethanayagam, R. Robert Freeman, Michael L. Singh, Keshav K. Ayyasamy, Vanniarajan Segal, Brahm H.
Description	Country affiliation: United States Author Affiliation: Davidson BA ( Department of Anesthesiology, University at Buffalo School of Medicine, Buffalo, NY 14214, USA.)
Abstract	Recruitment of neutrophils and release of reactive oxygen species are considered to be major pathogenic components driving acute lung injury (ALI). However, NADPH oxidase, the major source of reactive oxygen species in activated phagocytes, can paradoxically limit inflammation and injury. We hypothesized that NADPH oxidase protects against ALI by limiting neutrophilic inflammation and activating Nrf2, a transcriptional factor that induces antioxidative and cytoprotective pathways. Our objective was to delineate the roles of NADPH oxidase and Nrf2 in modulating acute lung inflammation and injury in clinically relevant models of acute gastric aspiration injury, a major cause of ALI. Acid aspiration caused increased ALI (as assessed by bronchoalveolar lavage fluid albumin concentration) in both NADPH oxidase-deficient mice and Nrf2(-/-) mice compared with wild-type mice. NADPH oxidase reduced airway neutrophil accumulation, but Nrf2 decreased ALI without affecting neutrophil recovery. Acid injury resulted in a 120-fold increase in mitochondrial DNA, a proinflammatory and injurious product of cellular necrosis, in cell-free bronchoalveolar lavage fluid. Pharmacologic activation of Nrf2 by the triterpenoid 1-[2-cyano-3-,12-dioxooleana-1,9 (11)-dien-28-oyl]imidazole limited aspiration-induced ALI in wild-type mice and reduced endothelial cell injury caused by mitochondrial extract-primed human neutrophils, leading to the conclusion that NADPH oxidase and Nrf2 have coordinated, but distinct, functions in modulating inflammation and injury. These results also point to Nrf2 as a therapeutic target to limit ALI by attenuating neutrophil-induced cellular injury.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1202410
Journal	The Journal of Immunology
Issue Number	4
Volume Number	190
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-02-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Acute Lung Injury Etiology Metabolism Inflammation Mediators Physiology Nadph Oxidase Nf-e2-related Factor 2 Enzymology Animals Cell Line, Tumor Disease Models, Animal Human Umbilical Vein Endothelial Cells Intubation, Intratracheal Mice Mice, 129 Strain Mice, Inbred C57bl Mice, Knockout Deficiency Neutrophil Infiltration Immunology Neutrophils Pathology Research Support, N.i.h., Extramural Research Support, U.s. Gov't, Non-p.h.s. Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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NADPH oxidase and Nrf2 regulate gastric aspiration-induced inflammation and acute lung injury

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NADPH oxidase and Nrf2 regulate gastric aspiration-induced inflammation and acute lung injury.

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NADPH oxidase and Nrf2 regulate gastric aspiration-induced inflammation and acute lung injury.