NDLI: Inhaled carbon monoxide accelerates resolution of inflammation via unique proresolving mediator-heme oxygenase-1 circuits.

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Developmental expression of IL-12Rß2 on murine naive neonatal T cells counters the upregulation of IL-13R 1 on primary Th1 cells and balances immunity in the newborn.

STAT4-dependent and -independent Th2 responses correlate with protective immunity against lung infection with Pneumocystis murina.

Inhaled carbon monoxide accelerates resolution of inflammation via unique proresolving mediator-heme oxygenase-1 circuits.

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What is and what should always have been: long-lived plasma cells induced by T cell-independent antigens.

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Inhaled carbon monoxide accelerates resolution of inflammation via unique proresolving mediator-heme oxygenase-1 circuits.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Chiang, Nan Dalli, Jesmond Choi, Augustine M. K. Mirakaj, Valbona Kibi, Megumi Serhan, Charles N. Shinohara, Masakazu
Description	Country affiliation: United States Author Affiliation: Chiang N ( Department of Anesthesiology, Perioperative and Pain Medicine, Center for Experimental Therapeutics and Reperfusion Injury, Harvard Institutes of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.)
Abstract	Resolution of acute inflammation is an active event accompanied by biosynthesis of specialized proresolving mediators (SPM). We employed a systems approach to determine the impact of CO in resolution active programs during self-limited inflammation in mice. Compared with ambient air, inhaled CO gas (250 ppm) significantly limited PMN infiltration (â ¼44%, 6 h) into peritoneum and shortened resolution interval from 4 to 2 h. We profiled exudate lipid mediators (LM) via metabololipidomics, CO reduced leukotriene B4 (21 ± 11 versus 59 ± 24 pg/mouse, 6 h), and elevated SPM including resolvin (Rv) D1 (27 ± 4 versus 16 ± 5 pg/mouse) and maresin 1 (26 ± 9 versus 15 ± 3 pg/mouse). With human macrophages, SPM (10 pM-10 nM) elevated heme oxygenase (HO)-1 (â ¼50%, 8 h). CO also enhanced HO-1 expression and accumulation of RvD1 and RvD5, an action reversed by blockage of a key SPM biosynthesis enzyme 15-lipoxygenase type 1. Compared with normoxia, CO increased â ¼30% phagocytosis of opsonized zymosan with human macrophage, which was further enhanced by SPM (â ¼100%). This CO increased phagocytosis was blocked by 15-lipoxygenase inhibition, and SPM stimulated phagocytosis was diminished by HO-1 inhibition. In murine peritonitis, both pre- and posttreatment with CO inhalation significantly increased macrophages carrying ingested apoptotic PMN in exudates and enhanced PMN apoptosis. Taken together, these results indicate that CO accelerates resolution of acute inflammation, shortens resolution intervals, enhances macrophage efferocytosis, and temporally regulates local levels of lipid mediator/SPM. Moreover, they provide proresolving mechanisms for HO-1/CO, which is part of the SPM-initiated resolution circuit.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1202969
Journal	The Journal of Immunology
Issue Number	12
Volume Number	190
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-06-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Carbon Monoxide Administration & Dosage Heme Oxygenase-1 Metabolism Inflammation Immunology Signal Transduction Animals Apoptosis Drug Effects Cells, Cultured Inflammation Mediators Macrophages Mice Neutrophils Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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