AIM:ToinvestigatethetryptaseandhistaminereleaseabilityofhumancolonmastcellsuponIgEdependentorindependentactivationandthepotentialmechanisms.METHODS:Enzymaticallydispersedcellsfromhumancolonswerechallengedwithanti-IgEorcalciumionophoreA23187,andthecellsupernatantsafterchallengewerecollected.Bothconcentrationdependentandtimecoursestudieswithanti-IgEorcalciumionophoreA23187wereperformed.TryptasereleasewasdeterminedwithasandwichELISAprocedureandhistaminereleasewasmeasuredusingaglassfibre-basedfiuorometricassay.RESULTS:Bothanti-IgEandcalciumionophorewereabletoinducedosedependentreleaseofhistaminefromcolonmastcellswithuptoapproximately60%and25%nethistaminereleasebeingachievedwith1μg/mLcalciumionophoreand10μg/mLanti-IgE,respectively.Dosedependentreleaseoftryptasewasalsoobservedwithuptoapproximately19ng/mLand21ng/mLreleaseoftryptasebeingachievedwith10μg/mLanti-IgEand1μg/mLcalciumionophore,respectively.Timecoursestudyrevealedthatbothtryptaseandhistaminereleasefromcolonmastcellsstimulatedbyanti-IgEinitiatedwithin10secandreachedtheirmaximumreleaseat6minfollowingchallenge.Pretreatmentofcellswithmetabolicinhibitorsabolishedtheactionsofanti-IgEaswellascalciumionophore.Tryptaseandhistaminerelease,particularlythatinducedbycalciumionophorewasinhibitedbypretreatmentofcellswithpertussistoxin.CONCLUSION:Bothanti-IgEandcalciumionophoreareabletoinducesignificantreleaseoftryptaseandhistaminefromcolonmastcells,indicatingthatthiscelltypeislikelytocontributetothepathogenesisofcolitisandothermastcellassociatedintestinaldiseases.
