Induction of tryptase and XXXX release from @entity1 colon mast cells by IgE dependent or independent mechanisms.

@entity1 @entity112 @entity1960 @entity460 @entity3365
AIM: To investigate the tryptase and @entity112 release ability of @entity1 colon mast cells upon IgE dependent or independent activation and the potential mechanisms. METHODS: Enzymatically dispersed cells from @entity1 colons were challenged with anti-IgE or @entity460 ionophore @entity3365 , and the cell supernatants after challenge were collected. Both concentration dependent and time course studies with anti-IgE or @entity460 ionophore @entity3365 were performed. Tryptase release was determined with a sandwich ELISA procedure and @entity112 release was measured using a glass fibre-based fluorometric assay. RESULTS: Both anti-IgE and @entity460 ionophore were able to induce dose dependent release of @entity112 from colon mast cells with up to approximately 60% and 25% net @entity112 release being achieved with 1 microg/mL @entity460 ionophore and 10 microg/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 microg/mL anti-IgE and 1 microg/mL @entity460 ionophore, respectively. Time course study revealed that both tryptase and @entity112 release from colon mast cells stimulated by anti-IgE initiated within 10 sec and reached their maximum release at 6 min following challenge. Pretreatment of cells with metabolic inhibitors abolished the actions of anti-IgE as well as @entity460 ionophore. Tryptase and @entity112 release, particularly that induced by @entity460 ionophore was inhibited by pretreatment of cells with pertussis toxin. CONCLUSION: Both anti-IgE and @entity460 ionophore are able to induce significant release of tryptase and @entity112 from colon mast cells, indicating that this cell type is likely to contribute to the pathogenesis of @entity1960 and other mast cell associated intestinal diseases.
