BACKGROUND: Monocyte-chemoattractant protein 1 (MCP-1) activates macrophages and increases the migration of monocytes into tissue during inflammation. It was hypothesized that MCP-1 expression is involved in intestinal inflammation. METHODS: MCP-1 protein was detected by immunohistochemistry and immunoprecipitation. Biological activity of MCP-1 was assessed using a chemotactic assay. MCP-1 messenger RNA (mRNA) levels were measured by quantitative reverse-transcription polymerase chain reaction. RESULTS: In normal mucosa, MCP-1 was predominantly present in surface epithelium. In contrast, inflamed mucosa from patients with ulcerative colitis or Crohn's disease contained multiple cells immunoreactive for MCP-1, including spindle cells, mononuclear cells, and endothelial cells. Furthermore, MCP-1 mRNA expression was markedly increased in inflamed intestinal biopsy specimens from patients with inflammatory bowel disease. MCP-1 was detected in isolated intestinal epithelial cells and in conditioned media from Caco-2 cells. Caco-2 cell-conditioned media stimulated monocyte chemotaxis activity that was inhibited by anti-MCP-1 antibodies. Constituitive MCP-1 mRNA levels in Caco-2 cells were up-regulated by interleukin 1 beta and down-regulated by dexamethasone. CONCLUSIONS: In addition to lamina propria macrophages, endothelial cells, and spindle cells, intestinal epithelial cells are able to produce MCP-1. MCP-1 is expressed constitutively in the intestinal colonic mucosa and is up-regulated during inflammation.
BACKGROUND:Monocyte-chemoattractant protein 1 (MCP-1) activates macrophages and increases the migration of monocytes into tissue during inflammation. It was hypothesized that MCP-1 expression is involved in intestinal inflammation. METHODS:MCP-1 protein was detected by immunohistochemistry and immunoprecipitation. Biological activity of MCP-1 was assessed using a chemotactic assay. MCP-1 messenger RNA (mRNA) levels were measured by quantitative reverse-transcription polymerase chain reaction. RESULTS: In normal mucosa, MCP-1 was predominantly present in surface epithelium. In contrast, inflamed mucosa from patients with ulcerative colitis or Crohn's disease contained multiple cells immunoreactive for MCP-1, including spindle cells, mononuclear cells, and endothelial cells. Furthermore, MCP-1 mRNA expression was markedly increased in inflamed intestinal biopsy specimens from patients with inflammatory bowel disease. MCP-1 was detected in isolated intestinal epithelial cells and in conditioned media from Caco-2 cells. Caco-2 cell-conditioned media stimulated monocyte chemotaxis activity that was inhibited by anti-MCP-1 antibodies. Constituitive MCP-1 mRNA levels in Caco-2 cells were up-regulated by interleukin 1 beta and down-regulated by dexamethasone. CONCLUSIONS: In addition to lamina propria macrophages, endothelial cells, and spindle cells, intestinal epithelial cells are able to produce MCP-1. MCP-1 is expressed constitutively in the intestinal colonic mucosa and is up-regulated during inflammation.
Authors: P Manousou; G Kolios; V Valatas; I Drygiannakis; L Bourikas; K Pyrovolaki; I Koutroubakis; H A Papadaki; E Kouroumalis Journal: Clin Exp Immunol Date: 2010-11 Impact factor: 4.330
Authors: T Spoettl; M Hausmann; M Herlyn; M Gunckel; A Dirmeier; W Falk; H Herfarth; J Schoelmerich; G Rogler Journal: Clin Exp Immunol Date: 2006-07 Impact factor: 4.330
Authors: Gerold Bongers; David Maussang; Luciana R Muniz; Vanessa M Noriega; Alberto Fraile-Ramos; Nick Barker; Federica Marchesi; Nanthakumar Thirunarayanan; Henry F Vischer; Lihui Qin; Lloyd Mayer; Noam Harpaz; Rob Leurs; Glaucia C Furtado; Hans Clevers; Domenico Tortorella; Martine J Smit; Sergio A Lira Journal: J Clin Invest Date: 2010-10-11 Impact factor: 14.808
Authors: T Jakobsson; L-L Vedin; T Hassan; N Venteclef; D Greco; M D'Amato; E Treuter; J-Å Gustafsson; K R Steffensen Journal: Mucosal Immunol Date: 2014-05-07 Impact factor: 7.313