IL-5 and TNF-alpha participate in recruitment of eosinophils to intestinal mucosa in ulcerative colitis

Dig Dis Sci. 2001 Sep;46(9):2004-9. doi: 10.1023/a:1010659803912.

Abstract

There is an increased influx of activated eosinophils to the intestinal mucosa in active ulcerative colitis, and an increased release of eosinophil-derived proteins, such as ECP, has also been observed. These findings indicate that eosinophils may contribute to tissue damage and intestinal inflammation in this disease. The relative importance of different chemotactic factors and the impact of steroid treatment on their effect in active ulcerative colitis are not known. We measured the eosinophil chemotactic activity in perfusion fluids from 11 patients with ulcerative colitis before and after steroid treatment and from 7 control patients. The effect of neutralizing antibodies to IL-5 and -8, RANTES, eotaxin, MCP-3, TNF-alpha, GM-CSF was investigated. The chemotactic activity was higher in perfusion fluids from patients than from controls (P = 0.0043). Anti-IL-5 (P = 0.005) and -TNF-alpha (P = 0.017) inhibited the activity in perfusion fluids obtained before treatment. Steroid treatment prevented the effect of all antibodies but had no significant effect on the chemotactic activity. The chemotactic activity correlated with the levels of eosinophil granule proteins in the perfusion fluids. In conclusion, in ulcerative colitis, eosinophils are attracted to the intestinal tissue by chemotactic factors, of which IL-5 and TNF-alpha may be the most prominent steroid-sensitive ones. The steroid-insensitive chemotactic activities remain unidentified.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Cell Movement / physiology
  • Chemotaxis, Leukocyte / physiology*
  • Colitis, Ulcerative / physiopathology*
  • Eosinophils / physiology*
  • Female
  • Humans
  • Interleukin-5 / physiology*
  • Intestinal Mucosa / physiology*
  • Male
  • Middle Aged
  • Tumor Necrosis Factor-alpha / physiology*

Substances

  • Interleukin-5
  • Tumor Necrosis Factor-alpha