VIP in inflammatory bowel disease: state of the art

Endocr Metab Immune Disord Drug Targets. 2012 Dec;12(4):316-22. doi: 10.2174/187153012803832576.


The pathogenesis of inflammatory bowel syndrome (IBD), which includes Crohn's disease (CD) and ulcerative colitis (UC) is poorly understood. However, an inflammatory component is a common hallmark. It has been suggested that CD principally involves Th1 and/or Th17 cells, while UC is considered to be more Th2 driven. Because vasoactive intestinal peptide (VIP) has emerged in the last decade as a putative candidate for the treatment of inflammatory diseases with a Th1 component, it may as well serve as a therapeutic target in CD. In addition, experiments using mice deficient in VIP or its receptors have revealed that the endogenously-produced VIP may participate in the regulation of immunity. The aim of the present review is to summarize the quite considerable array of data which suggests that the VIP-receptor system plays a key role in modulating multiple molecular and cellular players involved in IBD.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Humans
  • Inflammatory Bowel Diseases / drug therapy
  • Inflammatory Bowel Diseases / metabolism
  • Inflammatory Bowel Diseases / physiopathology*
  • Mice
  • Mice, Knockout
  • Receptors, Vasoactive Intestinal Peptide / biosynthesis
  • Receptors, Vasoactive Intestinal Peptide / physiology
  • Toll-Like Receptors / drug effects
  • Vasoactive Intestinal Peptide / genetics
  • Vasoactive Intestinal Peptide / physiology*
  • Vasoactive Intestinal Peptide / therapeutic use


  • Receptors, Vasoactive Intestinal Peptide
  • Toll-Like Receptors
  • Vasoactive Intestinal Peptide