沙眼衣原体感染对人乳头瘤病毒相关宫颈癌进程机制的影响研究  

Effect of Chlamydia Trachomatis on progress of the HPV-related cervical cancer

作　　者：卢立全 张晓雪 张爱[2] 吕盈盈 Lu Liquan;Zhang Xiaoxue;Zhang Ai;Lyu Yingying(Department of Clinical Laboratory,Shanghai Key Laboratory of Pathogenic Fungi Medical Examination,Shanghai Pudong New Area People′s Hospital,Shanghai 200137,China)

机构地区：[1]上海市浦东新区人民医院检验科、上海市病原真菌医学检验重点实验室,200137 [2]上海市浦东新区人民医院妇产科,200137

出　　处：《山西医药杂志》2025年第6期412-417,F0003,共7页Shanxi Medical Journal

基　　金：上海市浦东新区科经委民生项目(PKJ2022-Y40);浦东新区卫健委面上项目(PW 2022A-25)。

摘　　要：目的探讨沙眼衣原体(CT)通过免疫抑制增强人乳头瘤病毒(HPV)持续感染,而对宫颈癌发生发展的机制影响。方法收集32例CT/HPV共感染、48例HPV感染、30例CT感染和20名健康人。抗原呈递能力分析检测朗罕细胞(LCs)功能。免疫荧光染色方法检测LCs密度,蛋白质免疫印迹法(Western blot)分析检测LC内PI3K和MAPK信号传导系统,流式细胞术测定LCs表面活化标志物、T细胞亚群和细胞凋亡。结果CT/HPV共感染组的抗原呈递能力和LCs密度低于HPV和CT感染组(P<0.05),HPV感染组低于对照组(P<0.01)。LC内PI3K信号传导通路进一步激活,而与HPV和CT感染组相比,CT/HPV共感染组LCs内的MAPK通路表达下降,使CT/HPV共感染组的免疫抑制加深。与HPV感染和CT感染组相比,CT/HPV共感染组CD4^(+)T细胞减少(P<0.05);CD8^(+)T细胞减少,但差异无统计学意义;CT/HPV共感染组中CD4^(+)/CD8^(+)比率降低,T细胞凋亡增加。结论CT感染可通过降低LCs抗原递呈能力,影响PI3K和MAPK信号传导通路而抑制LCs功能,并且使CD4^(+)、CD8^(+)T细胞减少,凋亡增加,从而使HPV感染引起的免疫抑制加深,导致HPV持续感染,加快宫颈癌进程。Objective To explore the effect of Chlamydia trachomatis(CT)on human papillomavirus(HPV)persistence and how CT facilitates the progress of cervical cancer.Methods Thirty-two CT/HPV coinfections,48 HPV infections,30 CT infections,and 20 healthy individuals were collected.Langerhans cell(LC)function was detected by antigen-presenting ability analysis.Immunofluorescence staining was conducted to measure LC density and Treg infiltration.Moreover,Western blot analysis was performed to detect PI3K and MAPK signaling cascades.Flow cytometry was used to determine the surface activation markers on LCs,T cell subgroups,and apoptosis.Results The antigen presentation ability and LCs density in the CT/HPV coinfection group were lower than those in the HPV and CT infection groups(P<0.05),and those in the HPV infection group were lower than those in the control group(P<0.05).The PI3K signaling cascade was further activated,whereas the MAPK pathways were reduced in the CT/HPV coinfection group compared with the HPV and CT infection groups,leading to deeper immune suppression in the CT/HPV coinfection group.There was less CD4^(+)T cell and more Treg cell infiltration in the CT/HPV coinfection group than in the HPV and CT infection groups(P<0.05).CD8^(+)T cells became fewer in the CT/HPV group without significance,the CD4^(+)/CD8^(+)ratio was decreased and lymphocyte apoptosis was increased in the CT/HPV coinfection group compared to the HPV infection group.Conclusion CT infection can inhibit LCs function by reducing LCs antigen-presenting ability,affecting PI3K and MAPK signaling pathways,reducing CD4^(+)and CD8^(+)T cells,and increasing apoptosis,thus deepening immunosuppression caused by HPV infection,leading to continuous HPV infection and accelerating the process of cervical cancer.

关 键 词：沙眼衣原体 人乳头瘤病毒 郎格尔汉斯细胞 信号传导通路 免疫逃避 

分 类 号：R73[医药卫生—肿瘤]