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Vasoactive intestinal peptide dampens formyl-peptide-induced ROS production and inflammation by targeting a

P Chedid1,2,3, T Boussetta1,2,3, P M-C Dang1,2,3

  • 1Inserm, U1149, CNRS-ERL8252, Centre de Recherche sur l'Inflammation (CRI), Paris, France.

Mucosal Immunology
|June 9, 2016
PubMed

Insights

Vasoactive intestinal peptide (VIP) inhibits reactive oxygen species (ROS) production by phagocytes, specifically targeting the NOX2 enzyme. This peptide demonstrates anti-inflammatory effects by blocking key signaling pathways, suggesting its potential as a novel therapeutic agent.

Area of Science:

  • Immunology
  • Cell Biology
  • Pharmacology

Background:

  • Reactive oxygen species (ROS) are crucial for microbial clearance via phagocyte NADPH oxidase (NOX2) but can cause tissue damage when overproduced.
  • NOX2 is a complex enzyme involving membrane-bound cytochrome b588 and cytosolic components like p47phox, p67phox, p40phox, and rac1/2.

Purpose of the Study:

  • To investigate the effect of vasoactive intestinal peptide (VIP) on ROS production by NOX2 in human phagocytes.
  • To elucidate the signaling pathways and receptors involved in VIP's modulation of NOX2 activity.

Main Methods:

  • Primary human phagocytes were used to assess ROS production in response to bacterial peptide fMLF.
  • VIP's effects were analyzed using specific agonists and antagonists for VPAC1 receptors.
  • Western blotting was employed to examine the phosphorylation status of ERK1/2, p38MAPK, and p47phox.
  • An in vivo rat model of carrageenan-induced inflammation was used to evaluate VIP's anti-inflammatory properties.

Main Results:

  • VIP inhibited fMLF-induced ROS production in monocytes but not neutrophils.
  • VIP's inhibitory action was mediated via the VPAC1 receptor.
  • VIP suppressed the phosphorylation of ERK1/2, p38MAPK, and p47phox (Ser345).
  • VIP demonstrated significant anti-inflammatory effects in a rat model of acute inflammation.

Conclusions:

  • VIP acts as a natural anti-inflammatory agent, particularly within the mucosal system.
  • VIP inhibits NOX2 activation through the "MAPK-p47phox phosphorylation-NOX2 activation" pathway.
  • VIP and its analogs hold potential as novel therapeutic molecules for inflammatory conditions.

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