CAJ | 학술논문

目的通过检测病毒性心肌炎(VMC)小鼠和扩张型心肌病(DCM)患者的白介素17(IL,17)表达变化,研究IL-17在VMC和DCM中的表达.方法 100只雄性4周龄BALB/c小鼠分为VMC组(80只)和对照组(20只).以柯萨奇病毒B3(CVB3)感染小鼠建立VMC模型,RT-PCR法检测各时期小鼠脾细胞IL-17 mRNA表达水平,免疫组织化学法检测室肌组织IL-17蛋白表达.另选择30例DCM患者(DCM组),26例非DCM心脏病患者(非DCM组)及20例正常人(NC组),酶联免疫吸附法(ELISA)检测人血浆及外周血单个核细胞(PBMC)体外培养液中IL-17含量,并用RT-PCR法测定PBMC的IL-17 mRNA表达.结果 VMC小鼠脾细胞IL-17 mRNA在2周时无表达,4周后有表达,4及6周时表达均明显高于8周(P<0.01),VMC小鼠在2周时心室肌组织无IL-17蛋白表达,4周时心室肌组织中IL-17蛋白表达最高,6周至8周呈明显下降趋势(P<0.01).DCM组、非DCM组和NC组的血浆、PBMC自发培养上清液IL-17水平无显著性差异(P>0.05),但经植物抗血凝素(PHA)刺激培养后,DCM组PBMC培养上清液IL-17水平明显高于非DCM组和NC组(P<0.01).在DCM组、非DCM组和NC组直接提取及培养无刺激的PBMC中均无IL-17mRNA表达,经PHA刺激后DCM组PBMC中IL-17 mRNA表达明显高于非DCM组和NC组(P<0.05).结论小鼠病毒性心肌炎慢性期及扩张型心肌病患者IL-17表达明显增高,提示IL-17可能在VMC和DCM发病过程中起重要作用.
목적 통과검측병독성심기염(VMC)소서화확장형심기병(DCM)환자적백개소17(IL,17)표체변화,연구IL-17재VMC화DCM중적표체.방법 100지웅성4주령BALB/c소서분위VMC조(80지)화대조조(20지).이가살기병독B3(CVB3)감염소서건립VMC모형,RT-PCR법검측각시기소서비세포IL-17 mRNA표체수평,면역조직화학법검측실기조직IL-17단백표체.령선택30례DCM환자(DCM조),26례비DCM심장병환자(비DCM조)급20례정상인(NC조),매련면역흡부법(ELISA)검측인혈장급외주혈단개핵세포(PBMC)체외배양액중IL-17함량,병용RT-PCR법측정PBMC적IL-17 mRNA표체.결과 VMC소서비세포IL-17 mRNA재2주시무표체,4주후유표체,4급6주시표체균명현고우8주(P<0.01),VMC소서재2주시심실기조직무IL-17단백표체,4주시심실기조직중IL-17단백표체최고,6주지8주정명현하강추세(P<0.01).DCM조、비DCM조화NC조적혈장、PBMC자발배양상청액IL-17수평무현저성차이(P>0.05),단경식물항혈응소(PHA)자격배양후,DCM조PBMC배양상청액IL-17수평명현고우비DCM조화NC조(P<0.01).재DCM조、비DCM조화NC조직접제취급배양무자격적PBMC중균무IL-17mRNA표체,경PHA자격후DCM조PBMC중IL-17 mRNA표체명현고우비DCM조화NC조(P<0.05).결론 소서병독성심기염만성기급확장형심기병환자IL-17표체명현증고,제시IL-17가능재VMC화DCM발병과정중기중요작용.
Objective To explore the role of interleukin-17 (IL-17) in the evolution of viral myocarditis (VMC) into dilated cardiomyopathy (DCM). Methods A mouse model of VMC was established in 100 male Balb/c mice by intraperitoneal injection of coxsackievirus B3. The expression of IL-17 protein in the cardiac tissue of the mice was detected immunohistochemically, and IL-17 mRNA in the splenocytes was examined by reverse transcription-polyrnerase chain reaction (RT-PCR). IL-17 levels in the plasma, peripheral blood mononuclear cell (PBMC) culture supematants, and phytohemagglutinin (PHA)-stimulated PBMC culture supematants were measured in 30 DCM patients, 26 non-DCM patients and 20 normal adults using enzyme-linked immunosorbent assay (ELISA), and IL-17 mRNA expression in the PBMCs was detected using RT-PCR. Results The levels of IL-17 mRNA in the splenocytes of the mice with VMC were significantly higher at 4 and 6 weeks than those at 8 weeks (P<0.01), but not detected at 2 weeks. No IL-17 expression was found in the ventricular tissue of the mice at 2 weeks, but peaked at 4 weeks followed by gradual decrease (P<0.01). IL-17 level in PHA-stimulated PBMC culture supematants but not the plasma, and its mRNA level in PHA-stimulated PBMCs but not the PBMC culture supematants, were significantly elevated in DCM patients as compared with those in non-DCM patients and normal control subjects. Conclusion The mouse model of VMC in the chronic phase and DCM patients express high levels of IL-17, which may contribute to the transition from VMC to DCM.