{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T12:52:10Z","timestamp":1790254330638,"version":"4.1.0"},"reference-count":60,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2015,2,1]],"date-time":"2015-02-01T00:00:00Z","timestamp":1422748800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2015,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Diabetic complications involve inflammation-mediated microvascular and macrovascular damage, disruption of lipid metabolism, glycosylation of proteins, and abnormalities of neutrophil-mediated events. Resolution of inflamed tissues to health and homeostasis is an active process mediated by endogenous lipid agonists, including lipoxins and resolvins. This proresolution system appears to be compromised in type 2 diabetes (T2D). The goal of this study was to investigate unresolved inflammation in T2D. Wild-type (WT) and genetically engineered mice, including T2D mice (\n            <jats:italic>db<\/jats:italic>\n            \/\n            <jats:italic>db<\/jats:italic>\n            ), transgenic mice overexpressing the human resolvin E1 (RvE1) receptor (\n            <jats:italic>ERV1<\/jats:italic>\n            ), and a newly bred strain of\n            <jats:italic>db<\/jats:italic>\n            \/\n            <jats:italic>ERV1<\/jats:italic>\n            mice, were used to determine the impact of RvE1 on the phagocytosis of\n            <jats:named-content content-type=\"genus-species\">Porphyromonas gingivalis<\/jats:named-content>\n            in T2D. Neutrophils were isolated and incubated with fluorescein isothiocyanate-labeled\n            <jats:named-content content-type=\"genus-species\">P. gingivalis<\/jats:named-content>\n            , and phagocytosis was measured in a fluorochrome-based assay by flow cytometry. Mitogen-activated protein kinase (MAPK) (p42 and p44) and Akt (Thr308 and Ser473) phosphorylation was analyzed by Western blotting. The mouse dorsal air pouch model was used to evaluate the\n            <jats:italic>in vivo<\/jats:italic>\n            impact of RvE1. Results revealed that RvE1 increased the neutrophil phagocytosis of\n            <jats:named-content content-type=\"genus-species\">P. gingivalis<\/jats:named-content>\n            in WT animals but had no impact in\n            <jats:italic>db<\/jats:italic>\n            \/\n            <jats:italic>db<\/jats:italic>\n            animals. In\n            <jats:italic>ERV1<\/jats:italic>\n            -transgenic and\n            <jats:italic>ERV1<\/jats:italic>\n            -transgenic diabetic mice, phagocytosis was significantly increased. RvE1 decreased Akt and MAPK phosphorylation in the transgenic animals.\n            <jats:italic>In vivo<\/jats:italic>\n            dorsal air pouch studies revealed that RvE1 decreases neutrophil influx into the pouch and increases neutrophil phagocytosis of\n            <jats:named-content content-type=\"genus-species\">P. gingivalis<\/jats:named-content>\n            in the transgenic animals; cutaneous fat deposition was reduced, as was macrophage infiltration. The results suggest that RvE1 rescues impaired neutrophil phagocytosis in obese T2D mice overexpressing\n            <jats:italic>ERV1<\/jats:italic>\n            .\n          <\/jats:p>","DOI":"10.1128\/iai.02444-14","type":"journal-article","created":{"date-parts":[[2014,12,9]],"date-time":"2014-12-09T05:36:33Z","timestamp":1418103393000},"page":"792-801","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":80,"title":["Impact of Resolvin E1 on Murine Neutrophil Phagocytosis in Type 2 Diabetes"],"prefix":"10.1128","volume":"83","author":[{"given":"Bruno S.","family":"Herrera","sequence":"first","affiliation":[{"name":"Department of Applied Oral Sciences, Forsyth Institute, Cambridge, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hatice","family":"Hasturk","sequence":"additional","affiliation":[{"name":"Department of Applied Oral Sciences, Forsyth Institute, Cambridge, Massachusetts, 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