Intestinaldendriticcellschangeinnumberinfulminanthepaticfailure

摘要： AIM:Toinvestigatethechangeinintestinaldendriticcell(DC)numberinfulminanthepaticfailure(FHF).METHODS:AnanimalmodelofFHFwascreated.IntestinalCD11b/cwasdetectedbyimmunohistochemistryandWesternblot.Quantitativereal-timepolymerasechainreaction(PCR)wasusedtodetectintestinalintegrin-αmRNAexpression.IntestinalCD83,CD86,CD74,CD3andAKTweredetectedbyimmunohistochemistry,WesternblotandPCR.Phosphorylated-AKT(p-AKT)wasdetectedbyimmunohistochemistryandWesternblot.RESULTS:IntheFHFgroup[D-galactosamine(D-Galn)+lipopolysaccharide(LPS)group],themicebegantodieafter6h;conversely,intheD-GalnandLPSgroups,theactivityofmicewaspoor,buttherewerenodeaths.ImmunohistochemistryresultsshowedthatinFHF,theexpressionofCD11b/c(7988400±385941vs1102400±132273,P<0.05),CD83(13875000±467493vs9257600±400364,P<0.05),CD86(7988400±385941vs1102400±13227,P<0.05)andCD74(11056000±431427vs4633400±267903,P<0.05)wassignificantlyincreasedcomparedwiththenormalsaline(NS)group.ComparedwiththeNSgroup,theproteinexpressionofCD11b/c(5.4817±0.77vs1.4073±0.37,P<0.05)andCD86(4.2673±0.69vs1.1379±0.42,P<0.05)wassignificantlyincreased.Itg-α(1.1224±0.3vs0.4907±0.19,P<0.05),CD83(3.6986±0.40vs1.0762±0.22,P<0.05)andCD86(1.5801±0.32vs0.8846±0.10,P<0.05)mRNAexpressionwasincreasedsignificantlyintheFHFgroup.Attheproteinlevel,expressionofCD74intheFHFgroup(2.3513±0.52)wassignificantlyincreasedcomparedwiththeNSgroup(1.1298±0.33),whereasintheLPSgroup(2.3891±0.47),thelevelofCD74wasthehighest(P<0.05).Atthegenelevel,therelativeexpressionofCD74mRNAintheFHFgroup(1.5383±0.26)wasalsosignificantlyincreasedincomparisontotheNSgroup(0.7648±0.22;P<0.05).CD3expressionwasthehighestintheFHFgroup(P<0.05).IntheFHF,LPSandD-Galngroups,theexpressionofAKTattheproteinandmRNAlevelswaselevatedcomparedwiththeNSgroup,buttherewasnostatisticalsignificance(P>0.05).Thep-AKTproteinexpressionintheFHF(1.54±0.06),LPS(1.56±0.05)andD-Galn(1.29±0.03)groupswashigherthanthatintheNSgroup(1.07±0.03)(P<0.05).CONCLUSION:InFHF,alargenumberofDCsmature,expressCD86,andactivateMHCclassⅡmolecularpathwaystoinduceaTcellresponse,andtheAKTpathwayisactivated. ... （共11页）