NDLI: Specific role of neutrophil inducible nitric oxide synthase in murine sepsis-induced lung injury in vivo.

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Specific role of neutrophil inducible nitric oxide synthase in murine sepsis-induced lung injury in vivo.

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Specific role of neutrophil inducible nitric oxide synthase in murine sepsis-induced lung injury in vivo.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wang, Lefeng Taneja, Ravi Razavi, Habib Moshref Law, Cedrin Gillis, Christopher Mehta, Sanjay
Description	Country affiliation: Canada Author Affiliation: Wang L ( Program in Critical Illness Research, Lawson Health Research Institute, London, Ontario, Canada.)
Abstract	Nitric oxide produced by inducible nitric oxide synthase (iNOS) contributes importantly to acute lung injury (ALI), but the specific contribution of neutrophil iNOS has not been defined. Thus, we defined the role of neutrophils and specifically neutrophil iNOS in a murine model of septic ALI. Four hours after cecal ligation/perforation, ALI was characterized by increases in pulmonary neutrophil infiltration (tissue myeloperoxidase activity, bronchoalveolar lavage neutrophils), microvascular leak of Evans blue (EB) dye-labeled albumin, and oxidant stress (8-isoprostane levels). Septic ALI was neutrophil dependent, as pretreatment with anti-CD18 before cecal ligation/perforation significantly (P < 0.05) attenuated septic increases in pulmonary myeloperoxidase (39 ± 11 vs. 85 ± 14 mU/mg protein), bronchoalveolar lavage neutrophils (0.5% ± 0.2% vs. 2.1% ± 0.6%), microvascular EB-albumin leak (1.3 ± 0.3 vs. 2.6 ± 0.7 µg EB/g per minute), and 8-isoprostane content (74 ± 15 vs. 115 ± 16 pg/mg protein). The role of neutrophil iNOS was assessed by creation of neutrophil-iNOS chimeric mice: iNOS(+/+) versus iNOS(-/-) mice were bone marrow depleted by irradiation and selectively reconstituted with iNOS(+/+) versus iNOS(-/-) neutrophils. Cecal ligation/perforation resulted in significant septic ALI in + to - neutrophil-iNOS chimeric mice (iNOS(+/+) neutrophils in iNOS(-/-) mice), but not in - to + neutrophil depleted-reconstituted mice (iNOS(-/-) neutrophils in iNOS(+/+) mice). There were no significant differences between iNOS(+/+) and iNOS(-/-) neutrophils in phagocytosis, respiratory burst, or CD11a/b/CD18 surface expression, although septic shedding of CD62L was blunted in iNOS(-/-) neutrophils. Neutrophil iNOS contributes importantly to murine septic ALI in vivo, but not simply through a change in neutrophil phenotype. We speculate that neutrophil iNOS may modulate neutrophil-endothelial interactions in complex fashion, including regulation of transendothelial neutrophil migration and pulmonary neutrophil infiltration.
File Format	HTM / HTML
ISSN	10732322
Issue Number	5
Volume Number	37
e-ISSN	15400514
Journal	Shock
Language	English
Publisher	Lippincott Williams & Wilkins
Publisher Date	2012-05-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Intensive care medicine Acute Lung Injury Enzymology Neutrophil Infiltration Neutrophils Nitric Oxide Synthase Type Ii Metabolism Sepsis Genetics Pathology Animals Antigens, Cd Cell Movement Disease Models, Animal Endothelium, Vascular Male Mice Mice, Knockout Phagocytosis Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Emergency Medicine Critical Care and Intensive Care Medicine

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