Show simple item record

dc.contributor.authorAbdulnour, Raja Elie E.en_US
dc.contributor.authorSham, Ho Panen_US
dc.contributor.authorDouda, David N.en_US
dc.contributor.authorColas, Romain A.en_US
dc.contributor.authorDalli, Jesmonden_US
dc.contributor.authorBai, Yanen_US
dc.contributor.authorAi, Xingbinen_US
dc.contributor.authorSerhan, Charles N.en_US
dc.contributor.authorLevy, Bruce D.en_US
dc.date.accessioned2016-12-02T15:24:38Z
dc.date.issued2016en_US
dc.identifier.citationAbdulnour, Raja Elie E., Ho Pan Sham, David N. Douda, Romain A. Colas, Jesmond Dalli, Yan Bai, Xingbin Ai, Charles N. Serhan, and Bruce D. Levy. 2016. “Aspirin-triggered resolvin D1 is produced during self-resolving gram-negative bacterial pneumonia and regulates host immune responses for the resolution of lung inflammation.” Mucosal immunology 9 (5): 1278-1287. doi:10.1038/mi.2015.129. http://dx.doi.org/10.1038/mi.2015.129.en
dc.identifier.issn1933-0219en
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:29626055
dc.description.abstractBacterial pneumonia is a leading cause of morbidity and mortality worldwide. Host responses to contain infection and mitigate pathogen-mediated lung inflammation are critical for pneumonia resolution. Aspirin-triggered resolvin D1 (AT-RvD1; 7S,8R,17R trihydroxy-4Z,9E,11E,13Z,15E,19Z docosahexaenoic acid) is a lipid mediator that displays organ protective actions in sterile lung inflammation, and regulates pathogen-initiated cellular responses. Here, in a self-resolving murine model of Escherichia coli pneumonia, lipid mediator metabololipidomics performed on lungs obtained at baseline, 24 hours and 72 hours after infection uncovered temporal regulation of endogenous AT-RvD1 production. Early treatment with exogenous AT-RvD1 (1 hr post-infection) enhanced clearance of E.coli and Pseudomonas aeruginosa in vivo, and lung macrophage phagocytosis of fluorescent bacterial particles ex vivo. Characterization of macrophage subsets in the alveolar compartment during pneumonia identified efferocytosis by infiltrating macrophages (CD11bHi CD11cLow) and exudative macrophages (CD11bHi CD11cHi). AT-RvD1 increased efferocytosis by these cells ex vivo, and accelerated neutrophil clearance during pneumonia in vivo. These anti-bacterial and pro-resolving actions of AT-RvD1 were additive to antibiotic therapy. Taken together, these findings suggest that the pro-resolving actions of AT-RvD1 during pneumonia represent a novel host-directed therapeutic strategy to complement the current antibiotic centered approach to combatting infections.en
dc.language.isoen_USen
dc.relation.isversionofdoi:10.1038/mi.2015.129en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC5107310/pdf/en
dash.licenseLAAen_US
dc.subjectResolutionen
dc.subjectpneumoniaen
dc.subjectmacrophageen
dc.subjectlipid mediatoren
dc.subjectAT-RvD1en
dc.titleAspirin-triggered resolvin D1 is produced during self-resolving gram-negative bacterial pneumonia and regulates host immune responses for the resolution of lung inflammationen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalMucosal immunologyen
dash.depositing.authorDouda, David N.en_US
dc.date.available2016-12-02T15:24:38Z
dc.identifier.doi10.1038/mi.2015.129*
dash.contributor.affiliatedAi, Xingbin
dash.contributor.affiliatedDouda, David N.
dash.contributor.affiliatedSerhan, Charles
dash.contributor.affiliatedLevy, Bruce


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record