简介：Historically,mastcellswereknownasakeycelltypeinvolvedintypeIhypersensitivity.Untillasttwodecades,thiscelltypewasrecognizedtobewidelyinvolvedinanumberofnon-allergicdiseasesincludinginflammatoryboweldisease(IBD).MarkedlyincreasednumbersofmastcellswereobservedinthemucosaoftheileumandcolonofpatientswithIBD,whichwasaccompaniedbygreatchangesofthecontentinmastcellssuchasdramaticallyincreasedexpressionofTNFα,IL-16andsubstanceP.TheevidenceofmastcelldegranulationwasfoundinthewallofintestinefrompatientswithIBDwithimmunohistochemistrytechnique.ThehighlyelevatedhistamineandtryptaselevelsweredetectedinmucosaofpatientswithIBD,stronglysuggestingthatmastcelldegranulationisinvolvedinthepathogenesisofIBD.However,littleisknownoftheactionsofhistamine,tryptase,chymaseandcarboxypeptidaseinIBD.Overthelastdecade,heparinhasbeenusedtotreatIBDinclinicalpractice.Thelowmolecularweightheparin(LMWH)waseffectiveasadjuvanttherapy,andthepatientsshowedgoodclinicalandlaboratoryresponsewithnoseriousadverseeffects.TherolesofPGD2,LTC4,PAFandmastcellcytokinesinIBDwerealsodiscussed.Recently,aseriesofexperimentswithdispersedcolonmastcellssuggestedthereshouldbeatleasttwopathwaysinmanformastcellstoamplifytheirownactivation-degranulationsignalsinanautocrineorparacrinemanner.Thehypothesisisthatmastcellsecretogoguesinducemastcelldegranulation,releasehistamine,thenstimulatetheadjacentmastcellsorpositivelyfeedbacktofurtherstimulateitshostmastcellsthroughH1receptor.Whereasreleasedtryptaseactssimilarlytohistamine,butactivatesmastcellsthroughitsreceptorPAR-2.Theconnectionsbetweencurrentanti-IBDtherapiesorpotentialtherapiesforIBDwithmastcellswerediscussed,implicatingfurtherthatmastcellisakeycelltypethatisinvolvedinthepathogenesisofIBD.Inconclusion,whilepathoge