Potential clinical treatment of colitis with cardiotrophin-1

Clin Sci (Lond). 2018 Oct 18;132(20):2169-2174. doi: 10.1042/CS20171626. Print 2018 Oct 31.

Abstract

In a recent issue of Clinical Science, Prieto-Vicente et al. [Clin. Sci. (2018) 132, 985-1001] have smartly demonstrated a potential new use of cardiotrophin-1 (CT-1) to treat and palliate an inflammatory bowel disease such as ulcerative colitis. In that work, authors report that in ulcerative colitic mice, administration of exogenous recombinant CT-1 (rCT-1) promotes lower colon damage and lower disease activity index, reducing systemic levels of tumor necrosis factor α (TNF-α) and also diminishing TNF-α expression in colon together with the reduction in other common inflammation markers. Besides, in vivo rCT-1 administration induces activation of several molecular pathways, including nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) and signal transducer and activator of transcription (STAT)-3, and abolishes bacterial translocation from intestine to other organs, including mesenteric ganglia, lungs, and spleen. Additionally, these results were nicely corroborated in CT-1 depleted mice; in which colon damage and ulcerative colitis severity were greater compared with the wild-type counterparts. All together, these results suggested that CT-1 could be a promising new therapeutic approach for treating inflammatory bowel disease, particularly ulcerative colitis. However, further studies are required to determine its major mechanisms of action and the potential efficacy of CT-1 in human inflammatory bowel diseases.

Keywords: CT-1; inflammation; nuclear factor kappaB; ulcerative colitis.

Publication types

  • Comment

MeSH terms

  • Animals
  • Colitis*
  • Colitis, Ulcerative*
  • Colon
  • Dextran Sulfate
  • Humans
  • Mice
  • NF-kappa B

Substances

  • NF-kappa B
  • Dextran Sulfate