HIV／MTB 患者外周血单核细胞 TLR4表达和血浆 TNF-α水平检测

Expression of TLR4 in peripheral blood mononuclear cells and plasma concentrations of TNF-αin patients with HIV/MTB co-infection

目的：探讨HIV/MTB双重感染对外周血单核细胞TLR4及其信号通路下游因子TNF-α表达的影响。方法连续抽取在广西南宁市第四人民医院2012年1月至2013年1月就诊的HIV单纯感染者（32人）、HIV/MTB双重感染者（30人）、MTB单纯感染者（28人）、健康对照人群（29人）为研究对象，共119人，采集其外周20 ml静脉血，用流式细胞术检测外周血单核细胞TLR4表达水平、ELISA法测定血浆TNF-α浓度，同时测定HIV组和HIV/MTB组病毒载量；比较上述不同组间的指标差异。结果4组单核细胞TLR4 MFI 表达分别为21．62±4．67、18．29±3．87、16．79±4．45和22．85±5．80，4组间差异有统计学意义（F＝8．105，P＜0．01），MTB组和HIV/MTB组表达均比对照组低（P均＜0．01），MTB组和HIV/MTB表达比HIV组低（P＜0．01，P＝0．014）；4组血浆TNF-α浓度分别为15．892（10．494～21．646） pg/ml、13．142（8．014～22．038） pg/ml、16．284（11．916～24．005） pg/ml和26．657（16．321～34．541） pg/ml，4组间差异有统计学意义（F＝4．350，P＝0．006），HIV组和HIV/MTB组表达均比对照组低（P＝0．009和P＝0．001）。 HIV/MTB组的病毒载量为（5．113±1．018）拷贝/ml，HIV组为（4．416±1．020）拷贝/ml，两组比较差异有统计学意义（t＝3．449，P＝0．001）。结论 MTB可通过抑制TLR4信号通路来促进HIV的复制，HIV的感染可减少TNF-α分泌引起机体对MTB易感，从而促使HIV/MTB双重感染的发生。

Objective To investigate the expression of TLR 4 and its downstream factor TNF-αin the patients with human immunodeficiency virus and Mycobacterium tuberculosis （ HIV/MTB） co-infection. Methods A total of 119 subjects including 32 patients with HIV infection （HIV group）, 30 patients with HIV/MTB co-infection （HIV/MTB group）, 28 patients with MTB infection （MTB group） and 29 healthy subjects （ control group ） were recruited continuously from the Fourth People′s Hospital of Nanning City , Guangxi.The expression of TLR4 in peripheral blood mononuclear cells （PBMCs） from the patients was de-termined by flow cytometry .ELISA was performed to detect TNF-αin plasma samples .The HIV-1 viral load was determined by standard method .Results The mean fluorescence intensity （ MFI） for TLR4 expression in PBMCs from HIV, HIV/MTB, MTB and control groups were 21.62±4.67, 18.29±3.87, 16.79±4.45, and 22.85±5.80, respectively, showing significant differences among four groups （F=8.105, P〈0.01）. The TLR4 levels in MTB and HIV/MTB groups were significantly lower than those in control group （ both P〈0.01） and HIV group （P〈0.01, P=0.014）.The plasma concentrations of TNF-αin HIV, HIV/MTB, MTB and control groups were 15.892 （10.494-21.646） pg/ml, 13.142 （8.014-22.038） pg/ml, 16.284 （11.916-24.005） pg/ml, and 26.657 （16.321-34.541） pg/ml, respectively, that were significantly dif-ferent from each other （F=4.350, P=0.006）.The levels of TNF-αin plasma from patients with HIV and＆amp;nbsp;HIV/MTB infection were significantly lower than those of healthy subjects （P=0.009 and P=0.001）.The viral load in patients from HIV/MTB group （5.113 ±1.018 copies/ml） was significantly higher than that from HIV group （4.416±1.020 copies/ml） （t=3.449, P=0.001）.Conclusion MTB infection might promote HIV replication by inhibiting the expression of TLR 4.HIV infection might increase host′s suscepti-bility to MTB infection by reducing the production of TNF-α.Suppressed expression of TLR and TNF-αpro-duction could contribute to the occurrence of HIV /MTB co-infection .