PMID- 8566835 OWN - NLM STAT- MEDLINE DCOM- 19960304 LR - 20190501 IS - 0017-5749 (Print) IS - 1458-3288 (Electronic) IS - 0017-5749 (Linking) VI - 38 IP - 1 DP - 1996 Jan TI - Effect of c-kit ligand, stem cell factor, on mediator release by human intestinal mast cells isolated from patients with inflammatory bowel disease and controls. PG - 104-14 AB - The regulation of mediator release in human intestinal mast cells is largely unknown. Apart from IgE receptor crosslinking no secretagogues have been described so far. This study examined the effect of two cytokines (c-kit ligand and interleukin 3) and other agonists on human intestinal mast cell function. Cells were isolated from surgery specimens of 47 patients undergoing intestinal resection because of tumours or inflammatory bowel disease. Cell suspensions contained 3.6% mast cells (mean of 50 experiments). After preincubation without or with c-kit ligand or interleukin 3, cells were stimulated by IgE receptor crosslinking, C5a or formyl-methionyl-leucyl-phenylalanine (fMLP). Histamine and sulphidoleukotriene release was measured in supernatants. The sequential stimulation of the cells with c-kit ligand and IgE receptor crosslinking induced the release of high amounts of histamine and leukotrienes, whereas each agonist by itself induced only marginal mediator release. Interleukin 3 induced no release by itself, but enhanced the IgE receptor dependent release, possibly by an indirect mechanism. No significant mediator release was seen in response to C5a and fMLP, even if the cells were pretreated with c-kit ligand. The mediator release, particularly that of leukotrienes, was higher in cells isolated from actively inflamed tissue from patients with inflammatory bowel disease compared with controls. In conclusion, it was found that, apart from IgE receptor crosslinking, c-kit ligand and interleukin 3 regulate mediator release in human intestinal mast cells. The enhancement of mediator release by cytokines may be of particular relevance in the pathogenesis of inflammatory bowel diseases and food intolerance reactions. FAU - Bischoff, S C AU - Bischoff SC AD - Department of Gastroenterology and Hepatology, Medical School of Hannover, Germany. FAU - Schwengberg, S AU - Schwengberg S FAU - Wordelmann, K AU - Wordelmann K FAU - Weimann, A AU - Weimann A FAU - Raab, R AU - Raab R FAU - Manns, M P AU - Manns MP LA - eng PT - Comparative Study PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - Gut JT - Gut JID - 2985108R RN - 0 (Interleukin-3) RN - 0 (Leukotrienes) RN - 0 (Ligands) RN - 0 (Stem Cell Factor) SB - IM MH - Adult MH - Aged MH - Aged, 80 and over MH - Case-Control Studies MH - Cells, Cultured MH - Female MH - Histamine Release/*drug effects MH - Humans MH - Inflammatory Bowel Diseases/*metabolism MH - Interleukin-3/*pharmacology MH - Leukotrienes/metabolism MH - Ligands MH - Male MH - Mast Cells/*metabolism MH - Middle Aged MH - Stem Cell Factor/*pharmacology PMC - PMC1382987 EDAT- 1996/01/01 00:00 MHDA- 1996/01/01 00:01 PMCR- 1996/01/01 CRDT- 1996/01/01 00:00 PHST- 1996/01/01 00:00 [pubmed] PHST- 1996/01/01 00:01 [medline] PHST- 1996/01/01 00:00 [entrez] PHST- 1996/01/01 00:00 [pmc-release] AID - 10.1136/gut.38.1.104 [doi] PST - ppublish SO - Gut. 1996 Jan;38(1):104-14. doi: 10.1136/gut.38.1.104.