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dc.contributor.authorWang, Chin-Wei
dc.contributor.authorColas, Romain
dc.contributor.authorDalli, Jesmond
dc.contributor.authorArnardottir, Hildur
dc.contributor.authorNguyen, Daniel
dc.contributor.authorHasturk, Hatice
dc.contributor.authorChiang, Nan
dc.contributor.authorVan Dyke, Thomas E.
dc.contributor.authorSerhan, Charles
dc.date.accessioned2019-10-05T16:04:38Z
dc.date.issued2016
dc.identifier.citationWang, Chin-Wei, Romain A. Colas, Jesmond Dalli, Hildur H. Arnardottir, Daniel Nguyen, Hatice Hasturk, Nan Chiang, Thomas E. Van Dyke, and Charles N. Serhan. 2015. “Maresin 1 Biosynthesis and Proresolving Anti-Infective Functions with Human-Localized Aggressive Periodontitis Leukocytes.” Edited by B. A. McCormick. Infection and Immunity 84 (3): 658–65. https://doi.org/10.1128/iai.01131-15.
dc.identifier.issn0019-9567
dc.identifier.issn1070-6313
dc.identifier.issn1098-5522
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:41483456*
dc.description.abstractLocalized aggressive periodontitis (LAP) is a distinct form of early-onset periodontitis linked to periodontal infection with uncontrolled inflammation and leukocyte-mediated tissue destruction. The resolution of inflammation is an active process orchestrated by specialized proresolving lipid mediators (SPMs). Since the level of the Maresin pathway marker 14-hydroxy-docosa-hexaenoic acid (14-HDHA) was lower in activated peripheral blood from LAP patients, we investigated the Maresin 1 (MaR1) biosynthetic pathway in these subjects and its role in regulating phagocyte functions. Macrophages from LAP patients had a lower level of expression of 12-lipoxygenase (similar to 30%) and reduced MaR1 (LAP versus healthy controls [HC], 87.8 +/- 50 pg/10(6) cells versus 239.1 +/- 32 pg/10(6) cells). Phagocytosis by LAP macrophages was reduced similar to 40% compared to that of HC, and killing of periodontal pathogens, including Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, were similarly reduced. LAP neutrophils also displayed slower kinetics (similar to 30%) and decreased maximal phagocytosis (similar to 20% lower) with these pathogens than those of HC. The administration of MaR1 at 1 nM enhanced phagocytosis (31 to 65% increase), intracellular antimicrobial reactive oxygen species production (26 to 71% increase), bacterial killing of these periodontal pathogens (22 to 38% reduction of bacterial titers), and restored impairment of LAP phagocytes. Together, these results suggest that therapeutics targeting the Maresin pathway have clinical utility in treating LAP and other oral diseases associated with infection, inflammation, and altered phagocyte functions.
dc.language.isoen_US
dc.publisherAmerican Society for Microbiology
dash.licenseLAA
dc.titleMaresin 1 Biosynthesis and Proresolving Anti-infective Functions with Human-Localized Aggressive Periodontitis Leukocytes
dc.typeJournal Article
dc.description.versionVersion of Record
dc.relation.journalInfection and Immunity
dash.depositing.authorSerhan, Charles Nicholas::40628494470cc50c44bd3fc1053e7d94::600
dc.date.available2019-10-05T16:04:38Z
dash.workflow.comments1Science Serial ID 43503
dc.identifier.doi10.1128/IAI.01131-15
dash.source.volume84;3
dash.source.page658


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