PMID- 9472675 OWN - NLM STAT- MEDLINE DCOM- 19980303 LR - 20240316 IS - 0009-9104 (Print) IS - 1365-2249 (Electronic) IS - 0009-9104 (Linking) VI - 111 IP - 1 DP - 1998 Jan TI - IL-4, IL-10 and IL-13 down-regulate monocyte-chemoattracting protein-1 (MCP-1) production in activated intestinal epithelial cells. PG - 152-7 AB - Several studies have demonstrated that intestinal epithelial cells play a major role in the initiation and perpetuation of intestinal inflammation by secreting proinflammatory cytokines and chemokines. MCP-1 is suggested to be a chemokine that plays a major part during intestinal inflammation in inflammatory bowel disease (IBD). Immunoregulatory cytokines such as IL-4, IL-10 and IL-13 have been described to exert anti-inflammatory properties on various cell types. The aim of our study was to determine the effect of Th2 cytokines on the production of MCP-1 by activated intestinal epithelial cells. We examined Caco-2 cells as well as intestinal epithelial cells which were isolated from surgical specimens. Production of the chemokine MCP-1 was determined under stimulated and non-stimulated conditions. IL-4, IL-10 and IL-13 were added to stimulated epithelial cells under various culture conditions. Supernatants were analysed for cytokine concentrations using ELISAs. Under stimulation with physiological agents like IL-1beta or tumour necrosis factor-alpha (TNF-alpha), we observed markedly increased concentrations of MCP-1 in supernatants of Caco-2 cells and intestinal epithelial cells. IL-4, IL-10 and IL-13 all had the capacity to down-regulate the production of MCP-1 in Caco-2 cells as well as in freshly isolated epithelial cells. Caco-2 cells which were primed with Th2 cytokines 24 h before stimulation were subsequently decreased in their ability to be stimulated by IL-1beta or TNF-alpha for MCP-1 production. As MCP-1 has been shown to play a major role during intestinal inflammation, the in vitro suppression of MCP-1 in enterocytes suggests the in vivo use of regulatory cytokines in patients with active IBD. FAU - Kucharzik, T AU - Kucharzik T AD - Department of Medicine B, University of Munster, Germany. FAU - Lugering, N AU - Lugering N FAU - Pauels, H G AU - Pauels HG FAU - Domschke, W AU - Domschke W FAU - Stoll, R AU - Stoll R LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - Clin Exp Immunol JT - Clinical and experimental immunology JID - 0057202 RN - 0 (Chemokine CCL2) RN - 0 (Interleukin-13) RN - 130068-27-8 (Interleukin-10) RN - 207137-56-2 (Interleukin-4) SB - IM MH - Caco-2 Cells MH - Chemokine CCL2/*biosynthesis MH - Down-Regulation MH - Humans MH - Interleukin-10/*pharmacology MH - Interleukin-13/*pharmacology MH - Interleukin-4/*pharmacology MH - Intestinal Mucosa/immunology/*metabolism PMC - PMC1904856 EDAT- 1998/02/24 00:00 MHDA- 1998/02/24 00:01 PMCR- 1999/01/01 CRDT- 1998/02/24 00:00 PHST- 1998/02/24 00:00 [pubmed] PHST- 1998/02/24 00:01 [medline] PHST- 1998/02/24 00:00 [entrez] PHST- 1999/01/01 00:00 [pmc-release] AID - 10.1046/j.1365-2249.1998.00481.x [doi] PST - ppublish SO - Clin Exp Immunol. 1998 Jan;111(1):152-7. doi: 10.1046/j.1365-2249.1998.00481.x.