AIM:To investigate the tryptase and histamine releaseability of human colon mast cells upon IgE dependent orindependent activation and the potential mechanisms.METHODS:Enzymatically dispersed cells from humancolons were challenged with anti-IgE or calcium ionophoreA23187,and the cell supernatants after challenge werecollected.Both concentration dependent and time coursestudies with anti-IgE or calcium ionophore A23187 wereperformed.Tryptase release was determined with asandwich ELISA procedure and histamine release wasmeasured using a glass fibre-based fiuorometric assay.RESULTS:Both anti-IgE and calcium ionophore were ableto induce dose dependent release of histamine from colonmast cells with up to approximately 60% and 25% nethistamine release being achieved with 1 μg/mL calciumionophore and 10μg/mL anti-IgE,respectively.Dosedependent release of tryptase was also observed with upto approximately 19 ng/mL and 21 ng/mL release oftryptase being achieved with 10μg/mL anti-IgE and 1μg/mL calcium ionophore,respectively.Time course studyrevealed that both tryptase and histamine release fromcolon mast cells stimulated by anti-IgE initiated within 10sec and reached their maximum release at 6 rain followingchallenge.Pretreatment of cells with metabolic inhibitorsabolished the actions of anti-IgE as well as calciumionophore.Tryptase and histamine release,particularly thatinduced by calcium ionophore was inhibited by pretreatmentof cells with pertussis toxin.CONCLUSION:Both anti-IgE and calcium ionophore areable to induce significant release of tryptase and histaminefrom colon mast cells,indicating that this cell type is likelyto contribute to the pathogenesis of colitis and other mastcell associated intestinal diseases. AIM: To investigate the role of tryptase and histamine release ability of human colon mast cells upon IgE dependent or in dependent activation and the potential mechanisms. METHODS: Enzymatically dispersed cells from human colon were challenged with anti-IgE or calcium ionophore A23187, and the cell supernatants after challenge were collected. Both concentration dependent and time coursestudies with anti-IgE or calcium ionophore A23187 wereperformed.Tryptase release was determined with asandwich ELISA procedure and histamine release was measured using a glass fiber-based fiuorometric assay .RESULTS: Both anti-IgE and calcium ionophore were ableto induce dose dependent release of histamine from colonmast cells with up to about 60% and 25% nethistamine release are achieved with 1 μg / mL calcium ionophore and 10 μg / mL anti-IgE, respectively. Dose dependent release of tryptase was also observed with up to approximately 19 ng / mL and 21 ng / mL release of tryptase being achieved with 10 μg / mL anti-IgE and 1 μg / mL calcium ionophore, respectively.Time course studyrevealed that both tryptase and histamine release fromcol mast cells stimulated by anti-IgE initiated within 10sec and reached their maximum release at 6 rain following challenge. Retreatment of cells with metabolic inhibitorsabolished the actions of anti-IgE as well as calciumionophore.Tryptase and histamine release, particularly that induced by calcium ionophore was inhibited by pretreatment of cells with pertussis toxin. CONCLUSION: Both anti-IgE and calcium ionophore are able to induce significant release of tryptase and histaminefrom colon mast cells, indicating that this cell type is likelyto contribute to the pathogenesis of colitis and other mastcell associated intestinal diseases.