(08-01-15) The Impact of Resolvin E1 on Murine Neutrophil Phagocytosis in Type 2 Diabetes.

Herrera BS1, Hasturk H1, Kantarci A1, Freire MO1, Nguyen O1, Kansal S1, Van Dyke TE2.
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Abstract
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 pro-resolution system appears to be compromised in Type 2 diabetes (T2D). The goal of this study was to investigate unresolved inflammation in T2D. Wild type and genetically engineered mice, including T2D mice (db/db), transgenic mice over-expressing the human resolvin E1 (RvE1) receptor (ERV1) and a newly bred strain of db/ERV1 mice, were used to determine the impact of RvE1 on phagocytosis of Porphyromonas gingivalis (P. gingivalis) in T2D. Neutrophils were isolated, incubated with FITC-labeled P. gingivalis and phagocytosis measured in a fluorochrome based assay by FACS. MAPK (p42 and p44) and AKT (Thr308 and Ser473) phosphorylation were analyzed by Western blot. The mouse dorsal air pouch model was used to evaluate the in vivo impact of RvE1. Results revealed that RvE1 increased neutrophil phagocytosis of P. gingivalis in WT, but had no impact in db/db animals. In ERV1-transgenic and in ERV1-transgenic diabetic mice, phagocytosis was significantly increased. RvE1 decreased AKT and MAPK phosphorylation in the transgenic animals. In vivo dorsal air pouch studies revealed that RvE1 decreases neutrophil influx into the pouch and increases neutrophil phagocytosis of P. gingivalis 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 ERV1.

SOURCE: Infect Immun. 2014 Dec 8. pii: IAI.02444-14. [Epub ahead of print]

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