痤疮丙酸杆菌VIP免费

Propionibacteriumacnes-ReactiveTHelper-1CellsintheSkinofPatientswithAcneVulgaris存在于寻常痤疮患者皮肤中的痤疮丙酸杆菌T助细胞—1•TotheEditor:Acnevulgarisisthecommonestskindisordertoaffecthumans,characterizedbybothnoninfammatory(comedones)andinflammatorylesions(papules,pustules,andnodulocysticlesions).Itisadiseaseofthepilosebaceousfolliclewithcomedonesresultingfromthehypercornificationofthekeratinocytesoftheductwallandusuallyprecedinginflammatorylesions(Cunliffeetal,2000).寻常痤疮是最普通的能影响人体健康的皮肤紊乱疾病，既有非发炎性（如粉刺）又有发炎性（如丘疹、脓包、结囊肿损害）损害特点，这是一种毛皮脂腺囊疾病，输送管壁的角蛋白超角质化或上面提到的发炎性损害导致了粉刺的形成（Cunliffeetal，2000）•OfparticularinterestinthepathophysiologyofinflammatoryacneistheroleofthenormalskincommensalbacteriumPropionibacteriumacnes.Althoughnotarequirementforcomedogenesis,anumberofobservationshavesuggestedthatP.acnesisimplicatedinthepathogenesisofinflammatoryacne.至于病理生理学上的发炎性损害，正常皮肤共生的细菌—丙酸杆菌粉刺起着特殊作用，尽管并不需要分生孢子，但是通过观察发现丙酸杆菌粉刺和感染性损害的发病机制有关系•ThedensityofP.acnesincreasesmarkedlyduringpubertycoincidingwiththeonsetofthedisease(Leydenetal,1975).P.acnesisrarelyfoundinanimalskinandacneisnotseeninanimals(Websteretal,1981;Kearneyetal,1982).TreatmentsthatreduceP.acnesnumbersleadtoclinicalimprovementofacne(Thiboutot,1997)and,finally,theemergenceofantibiotic-resistantP.acnesstrainsarelinkedtothefailureofantibiotictreatment(Eadyetal,1989).该病始于青春期，此间丙酸杆菌分析的数量显著增加，很少在动物皮肤发现丙酸杆菌痤疮，在动物体内也无发现痤疮，试图通过临床试验减少痤疮丙酸杆菌数量，抗生素疗法因为产生了抵抗抗生素的菌株而失败（Eadyetal，1989），•TheimmunostimulatoryactivityofP.acnesandresultingprototypicThelper1immuneresponsehasbeenwidelystudiedinanimalmodels(Matsuietal,1997;Okazakietal,2001);however,thespecificityandcytokineprofilesoflesionalTcellsfromskinofacnepatientshavenotbeeninvestigatedpreviously已经利用动物模型对痤疮丙酸杆菌引起的免疫活动和由原T助细胞引发的免疫应答进行了广泛的研究，然而还没有对痤疮病人皮肤受损害的T细胞原型及细胞因子原型的研究，•HerewedescribethegenerationofTcelllines(TCL)frominflamedacnelesions,and,theirproliferativeandcytokineresponsestoP.acnesantigens.ApprovalwasgrantedforthisresearchprojectbytheHammer-smithQueenCharlotte’s&ChelseaandActinHospitalsResearchEthicsCommittee.Fullconsentwasgrantedbysubjects这里我们将描述TCL的产生、增值以及细胞因子对痤疮丙酸杆菌抗原的免疫反应。•FourteenTCLweregeneratedfromearlypapularinflammatoryacnelesionsof16untreatedpatients,stainedforCD4,CD8,andTcellreceptorαβexpressionandtestedinproliferationassayswithP.acnesandcontrolantigens.Todeterminetheircytokineprofile,TCLwerestimulatedwithphorbal12-myristate13-acetate(PMA)plusionomycinorP.acnesextractandstainedintracellularlyforinterferon(IFN)-γ,interleukin(IL)-4,IL-5,andIL-10usingfowcytometry.ResultswerecomparedwitheightcorrespondingTCLgeneratedinthesamewayfromlesionalskinof11psoriaticpatients.十四TCL取自于16位未经处理的患早期丘疹感染损害的病人，CD4、CD8染色，T细胞受体αβ表达，增值实验检测P.粉刺与控制抗原（图1），为了确定细胞因子原型，以流式细胞术刺激TCL，用PMA加离子霉素或P.粉刺提取物以及细胞内的染色γ干扰素、白细胞介素（IL）—4、IL—5、IL—10，结果与采用相同方式从11位牛皮癣患者取出的8个TCL分析结果相比较。•AcneTCLconsist...