Anti-inflammatory action of angiotensin 1-7 in experimental colitis may be mediated through modulation of serum cytokines/chemokines and immune cell functions


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Abstract

We recently demonstrated Ang 1–7 reduced inflammation in the dextran sulfate sodium (DSS) colitis model. In this study we examined the effect of Ang 1–7 on modulation of plasma levels of selected cytokines and chemokines and immune cell effector functions (apoptosis, chemotaxis and superoxide release) in vitro. The degree of neutrophil recruitment to the colon was assessed by immunofluorescence and myeloperoxidase activity. Daily Ang 1–7 treatment at 0.01 mg/kg dose which previously ameliorated colitis severity, showed a significant reduction in circulating levels of several cytokines and chemokines, and neutrophil recruitment to the colonic tissue. It also significantly enhanced immune cell apoptosis, and reduced neutrophil chemotaxis and superoxide release in vitro. In contrast, daily administration of the Ang 1–7R antagonist A779 which previously worsened colitis severity showed significant up-regulation of specific mediators. Our results demonstrate a novel anti-inflammatory action of Ang 1–7 through modulation of plasma levels of cytokines/chemokines and immune cell activity.HighlightsWe have previously reported that Ang 1–7 treatment significantly reduced colitis severity at gross and histological levels.In the present report, we tested the mechanism (s) of the anti-inflammatory properties of Ang 1–7 using the DSS model.A significant reduction in circulating levels of selected cytokines and chemokines was shown by Ang 1–7 treatment.Treatment with the MAS-R antagonist A779 (worsened colitis severity) increased the levels of various cytokines/chemokines.Reduced degree of neutrophil recruitment to the colonic tissue was also shown by Ang 1–7 treatment.Ang 1–7 significantly enhanced immune cell apoptosis, and reduced neutrophil chemotaxis and superoxide release in vitro.

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