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Dietary fish oil reduces the acute inflammatory response and enhances resolution of antigen-induced peritonitis
Authors:Valgerdur Tomasdottir  Arnor Vikingsson  Jona Freysdottir  Ingibjorg Hardardottir
Affiliation:1. Department of Biochemistry and Molecular Biology, Biomedical Center, University of Iceland, 101 Reykjavik, Iceland;2. Department of Immunology, Faculty of Medicine, Biomedical Center, University of Iceland, 101 Reykjavik, Iceland;3. Center of Rheumatology Research and Department of Immunology, Landspitali – The University Hospital of Iceland, Reykjavik, Iceland
Abstract:Dietary n-3 polyunsaturated fatty acids (PUFA) influence the inductive phase of inflammation but less is known about their effects on the resolution phase. This study examined the effects of dietary fish oil on induction and resolution of antigen-induced inflammation in mice. Mice were fed a control diet with or without 2.8% fish oil, immunized twice with methylated BSA (mBSA) and inflammation induced by intraperitoneal injection of mBSA. Prior to and at different time points after mBSA administration, peritoneal cells were analyzed and expression of surface molecules determined by flow cytometry. Concentration of chemokines, cytokines and soluble cytokine receptors was determined by ELISA. Mice fed the fish oil diet had fewer peritoneal neutrophils, shorter resolution interval and lower levels of pro-inflammatory cytokines and chemokines than mice fed the control diet. In mice fed the fish oil diet there was an early peak in peritoneal levels of the immunosuppressive molecules sIL-6R and TGF-β, that was not seen in mice fed the control diet. In the resolution phase, peritoneal macrophages from mice fed the fish oil diet expressed more of the atypical chemokine receptor D6 and peritoneal TGF-β levels were higher than that in mice fed the control diet. Furthermore, in the late-resolution phase there were more peritoneal eosinophils and macrophages in mice fed the fish oil diet than in mice fed the control diet. These results demonstrate a suppressive effect of n-3 PUFA on the inductive phase of inflammation and indicate an enhancing effect of n-3 PUFA on resolution of inflammation.
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