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Study_4

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Study_4

    Study

27卷第4

    ;2001

    ;白求恩医科大学

    ;J.N.BETHUNEUNIV.MED.SCI.

    ;Vo1.27No.4

    ;2001

    ;[ArticleID]0253-3707(2001)040374-03

    ;StudyonrelationamongslCAM-1levelchangeinthepatientswith

    ;chronicviralhepaticdisease,viralreplication ;andtheclinicalsignificance

    ;LIDong-fu,JINZhen-jing,MENGXian-ming,PANLiuInn,WANGLi-yi

    ng,TAIJing-hun

    ;(Dept.ofDigestiveMedicine,SecondHospital,JilinUniversity,Changchun

    130041Chino)

    ;~Abstract]Objective:ToobserverelationamongslCAM

    1levelintheseraofpatientswithchronic ;viralhepaticdisease,viralreplicationandtheclinicalslgnificance.MethodsT

    helevelchangesof

    ;sIcAM1,IL-1,IL

    8andTNFaintheseraofpatientswithchronichepatitisB(CH),chronicsevere ;hepatitisB(CSH)andhepatocirrhosis(HC)weredetectedbyELIsA.Results:ThelevelsofsiCAM-

    ;1,IL1,IL

    8andTNFainseraotthepatientswithchronicviralhepaticdiseaseweresignificantly

    ;higherthanthoaeofhealthycontrolgroup(P<O.01).Thebilirubinlevelintheseraofpatientswith

    ;chronicviralhepaticdiseaseoldifferentclinicaltypespositivelycorrelatedwithsICAM1andcytokine

    ;activities.ThesICAM

    1levelintheseraofHBVDNAorHBeAgpositivepatientswassignificantly

    ;higherthanthoseofnegativepatients(P<O.05,P<O.01).Conclusion:TlhesICAM1levelandactivi

    ;tiesofcytokineIL.1.IL.8andTNFaaswellasthehilirubinleve],intheseraofthepatientscanreflect

    ;thenecrosisdegreeofhepatocytes,andthesICAM

    1levelandactivitiesofIL1,IL8andTNFawere

    ;relatedtostateofHBVcarrierortheactivedegreeofHBVinpatientswithhepaticdisease.

    ;[‘Keywords~chronicviralhepaticdisease;intercellularadhesionmolecule1}cylokineIL1,IL8,

;TNF

    ;[‘CLCnumber]R512.6}R373[Documentcode]A

    ;[摘要]目的:探讨慢性肝病患者血清可溶性粘附分子(siCAM)水平与

    病毒复制及临床关系方法;

    ;ELISA法对慢性肝病患者血清siCAM,炎症相关性细胞因子白细

    胞夼素-1(IL-1),白细胞夼素.8

    ;(IL-8)及肿瘤坏死因子(TNFa)水平进行了平行测定.结果t慢性肝病

    患者血清siCAM1,IL.1,IL8

    ;TNFa水平明显高于健康对照组I慢性乙型肝炎HBVDNA

    HBeAg阳性惠者明显高于HBvDNA

    ;HBeAg阴性惠者,且与血清总胆红素含量呈正相关.结论:siCAM

    1和炎症相关性细胞因子水平与

    ;慢性肝病志者病情及携带船V的活跃程度相关.

    ;Nowitwasknownthatintercellularadhesionmolecule1(ICAM

    1)wascloselyrelatedtothecourseof

    ;cellularadhesion,invadingandtransendothelialmovement.Solubleintercellularadhesionmolecule-1(slCAM.

    ;1)levelwashigherintheseraofmanypatientswithautoimmunohepatitis,andslCAM1inmanyinflammatory

    ;diseasehadbeenusedasimportantimmunologicalobservationalindex.StudyonrelationbetweenslCAM1lee

    ;elchangeandchronichepaticdiseasewasnotedbyinternat/onalandnationalr

esearchers.Therelationbetween

    ;[Reeelveddate]2000-07-08

    ;[Biography]LIDong-fu(1955--),male,borninYushuCity,JilinProvince,associateprofessor,graduatedfromDepartment0iMi

    ;crobiologyandImmunologyofBethuneUniversityofMedi~lSciencesa8postgraduatein1985.majoringindigestive

    ;systemtumoradoptiveimmunotherapyandgenetherapy,having53pepsrsand1bookpublished.

    ;374

    ;

    ;LIDongfu?etalStudyonrelationamongsICAM1levelchangeinthe’

    

    ;regularruleofslCAM

    1levelchangeandstatesofHBVcarrierandpatientSconditionwasstudiedinthispa

    ;per

    ;1Materialsandmethods

    ;SixtytwoserumspecimensofpatientswithhepatitisBwereobtainedinDepartmentofDigestive

    ;Medicine,SecondHospita1,JilinUniversity.Ofthe62patients,28patientswithhepatitisB,20malesand8fe

    ;males,meanagebeing41.6t10patientswithchronicseverehepatitisB,7male

sand3females,meanage39.6{

    ;24patientswithcirrhosisofliver,18malesand6females?meanage53.2.Allpatientswerediagnosedaccord

    ;ingtovira1hepatitistreatmentprogramrevisedinfifthnationa1meetingaboutinfectiveandparasiticdisease.

    ;Twentynormalpeolewhoal1volunteeredtodonatebloodwereascontro1group,15malesand5females,mean

    ;agebeing32.1.

    ;DetectingsICAMandcellularfactorreagentkitwereprovidedbyBoehringerMannheimandGenzyme

    ;Company.TheslCAM1,IL

    1,IL-8andTNFalevelchanges,andHBVserummarkerintheseraofpatients ;withchronichepaticdiseaseweredetectedbyELISAmethods,HBVDNA

    byPCRmethodsandTBjdby1”OO—

    ;finedeterminingmethod.

    ;2Results

    ;ParallelingdetectionofslCAM-1,IL1,IL

    8andTNFainseraofpatientswithHBVhepaticdiseasewas

    ;showninTable1.

    ;ComparisonofdetectingslCAM1,ILl,IL

    8andTNFaresultsbetweenchronichepatitispatientswith

    ;HBVDNAorHBeAgpositiveandpatientswithHBVDNAorHBeAgne

gativewasshowninTable2.

    ;Relationshipbetweenbilirubinleve1andtheactivitesofsICAM1,IL1,IL8andTNFainseraofpatients

    ;withchronicHBVhepaticdiseasewasshowninTable3.

    ;Tab.1ParallelingdetectionofslCAM1,IL1,IL8andTNFainseraofpatientswithchronicHBVhep

    ;aticdisease(;)

    ;*P<0.01comparedthhealthydor-0

    ;Tab2ComparisonofdetectingslCAM1,IL1,IL8andTNFaresultsbetweenchronichepatitispatients

    ;withHBVDNAorHBeAgpositiveandpatientswithHBVDNAorHBeAgnegative(;s)

    ;*P<0?05,P<0?01compa~dwithHBVDNA0rHBenegativegroup ;375

    ;

    ;自求恩医科大学2001年第27卷第4

    ;Tab.3RelationshipbetweenbilirubinlevelandtheactivitesofslCAM1.IL1.IL8andTNFainthesera

    ;ofpatientswithchronicHBVhepaticdisease(;)

    ;P(O?01comparedwithbillrubinevelbelow84pmol/Lgroup ;3Diseussion

    ;ExpressionofICAM

    1onnormalhepatocytewasinsufficientandtherewassmallamountofexpressionof

    ;ICAM

    1onhepaticsinusoidendothelialandvascularendotheliacells[?.ICAM1couldbindlymphocytefunc.

    ;tion-associatedantigen1(LFA

    1)onlymphocytemembrane.ItwasimportantthatLFA1onlymphocyte

    ;membranecombinedICAM

    1onthetargetcellmembranewhenliverwasattackedbyHBV,causinghepacellu

    ;lardegenerationandnecrosis,lymphocyteandtargetcellinteractionincludingcytotoxicTlymphocyte(CTL)

    ;andhepatocyteinfected.TheresultsofthisstudyshowedthatlevelsofsICAM1,IL1,IL8andTNFainthe

    ;seraofpatientswithchronicviralhepaticdiseaseweresignificantlyhigherthanthoseofhealthycontrolgroup

    ;(

    <0.01)andtherewasapositiverelationbetweenthehilirubinlevelintheseraofpatientswithchronicdif.

    ;ferentclinictypehepaticdiseaseandslCAM

    1,cytokineactivities.CytotoxicactionmediatedbyCTLwasan ;importantcauseofhepatocellulardegenerationandnecrosisduringHBVhep

aticdiseasedevelopment.HLAand

    ;ICAM-1expressiononhepatocytemembraneattackedbyHBVincreased.AsolubleICAM1(slCAM1)in

    ;seramainlyoriginatedfromthreeways:?

    hepatocellularmembranereleasing,?hepatocellularmembrane

    ;fallingdown,?

    hepatocellulaimembraneselfsecreting.Therefore,withincertainrangeslCAM1levelinsera

    ;couldreflecthepaticfunctioninjurydegree,andthisconclusionwasprovedinthisstudybyanalyzingrelation

    ;betweensICAM

    1levelandbilirubinincreasingdegree.ThisresultsalsoshowedthatslCAM

    1levelinthesera

    ;ofHBVDNAorHBeAgpositivepatientswassignificantlyhigherthanthatofnegativepatients,suggestingthat

    ;ICAMamountreleasedonhepatocellularmembraneincreasedbecauseofHBVproliferationinhepatocytesand

    ;hepatocellulardegenerationandnecrosis.TheresultsinthisstudyalsoindicatedthattheactivitiesofIL1.IL8

    ;andTNFaweresignificantlyhigherthanthoseofnormalcontrolgroup.IL

    1,IL8andTNFawereallinflam.

    ;matorycellularfactorsandmediatedinflammatoryreaction.Nowitwasknow

nthatIL.1couldstimulatepro.

    ;ductionofmononuclearleukocytechemotacticpeptide.1(MCP

    1)thatcouldpromotesynthesisofICAM.1133.

    ;IL

    8hadchemotactic,activatingmononuclearleukocyteandgranulocyteaction.TNFacouldcauselocalinflam

    ;matoryreactionandmultiorgandamage.I11,IL

    8andTNFa,inflammatorycellularfactors,notonlymediated ;hepatocellularimmunodamagebutalsoinducedICAM

    1expressiononhepatocytemembrane[‘].Therefore,

    ;multidetectingsICAM

    1andinflammatorycellularfactorshadsomesignificanceindeterminingthedegreeof

    ;chronichepaticdisease,statesofHBVcarrierandtheprognosis. ;[References]

    ;[1]HorlikeN,OnilM.KumonI.eta1.Intercellularadhesionmole:ule?1expressiononthehepatocytemembraneofpatientsBandc[J]Liver,1993, ;13:10-12.

    ;[

    Vo~pesR?VanDenDordjj,DesmetVJ.He~tlcexp~sslonofinte~ellularadhesionmolecule1(ICAM)inviralhepatitisB[J].Hematology.

    ;1990.12I148?151.

    ;Is]YanmaguchiY,MatsumuraF,TakeyaM.eta1.Monocylechemoattraclantp…otei1…hncxprein0finter?III…dhesionm.lI1fo1

    ;1owi~ischemioreperf~sianoftheliverinrats[J]_Hepatology.1998,27;727731.

    ;[4]MarltaM,WatanabeY,AkaideT,eta1.Inflammatoryeytokinesup.~gu[ateinte~ellularadhesionmolece[e.1ex9ion.priary[tured

    ;MsehepatocytesandT[mphocyteadhesion[J].Hepatology.1994,19:426

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    ;

    ;376

    ;

    ;

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