结核分枝杆菌感染环境中不同细胞因子对胸膜间皮细胞增殖和凋亡的影响
결핵분지간균감염배경중불동세포인자대흉막간피세포증식화조망적영향
Effects of different cytokines on proliferation and apoptosis of pleural mesothelial cells in human Mycobacterium tuberculosis infection
  • 万方数据
    中华结核和呼吸杂志 중화결핵화호흡잡지
    Chinese Journal of Tuberculosis and Respiratory Diseases
    2013年 5期 341-345 ,共5页

    熊亮%向菲%周琼%张建初

    웅량%향비%주경%장건초

    胸膜%上皮细胞%结核%胸腔积液 胸膜%上皮細胞%結覈%胸腔積液
    흉막%상피세포%결핵%흉강적액
    Pleura%Epithelial cells%Tuberculosis%Pleural effusion
    目的 探讨结核感染时不同细胞因子[IL-22、IL-17、γ干扰素(IFN-γ)]对胸膜间皮细胞(PMC)增殖和凋亡的影响.方法 应用流式细胞术检测PMC表面细胞因子受体IL-22R、IL-17R和IFN-γR1的表达；检测IL-22、IL-17、IFN-γ以及IFN-γ与IL-22或IL-17组合对PMC中的Ki-67表达和凋亡的影响；检测结核性胸腔积液(TPE)及其分别与抗IL-22、IL-17、IFN-γ单抗组合对PMC中的Ki-67表达的影响.结果 (1)结核分枝杆菌感染时PMC表面高表达IL-22R、IL-17R和IFN-γR1[PMC的阳性比例分别为(86.2±2.9)％、(41.5±4.4)％和(64.9±5.8)％]；(2)IL-22、IL-17组Ki-67阳性PMC细胞百分数分别为(31.5±2.0)％、(26.1±2.4)％,高于培养基组的(14.6±0.7)％(q值分别为6.8和4.9,均P＜0.05)；IFN-γ组为(5.2±1.2)％,低于完全培养基组(q=5.0,P＜0.05)；而IFN-γ+IL-22组为(23.4±1.7)％,IFN-γ+ IL-17组为(21.8±3.8)％,均高于IFN-γ组(q值分别为7.3和6.7,均P＜0.05).单独加入TPE或加入含有同型对照IgG的TPE组分别为(63±9)％、(63±11)％,均高于完全培养基组(q值分别为19.6和19.7,均P＜0.05)；TPE加入抗IFN-γ单抗之后为(82±4)％,高于TPE+ IgG组(q=7.5,P＜0.05);TPE加入抗IL-22单抗后为(34±3)％,低于TPE+ IgG组(q=11.8,P＜0.05)；TPE加抗IL-17单抗组为(58±5)％,与TPE+ IgG组差异无统计学意义(q=2.1,P ＞0.05).(3) IFN-γ组PMC凋亡率为(19.3±1.1)％,高于完全培养基组(4.3±0.6)％(q=33.4,P ＜0.05)；IL-22、IL-17组凋亡率分别为(3.8±0.6)％和(5.7±0.8)％,与完全培养基组差异无统计学意义(q值分别为1.3和3.0,均P＞0.05).IFN-γ+IL-22组凋亡率为(6.5±0.7)％,IFN-γ+ IL-17组为(8.7±1.7)％,均低于IFN-γ组(q值分别为28.5和23.6,均P＜0.05).结论 IL-22和IL-17促进PMC增殖而不导致其凋亡,并且能逆转IFN-γ对PMC增殖的抑制作用,以及逆转IFN-γ对PMC凋亡的诱导作用；结核分枝杆菌感染环境可促进PMC增殖,该效应可能与TPE中IL-22、IL-17和IFN-γ的综合作用有关.
    목적 탐토결핵감염시불동세포인자[IL-22、IL-17、γ간우소(IFN-γ)]대흉막간피세포(PMC)증식화조망적영향.방법 응용류식세포술검측PMC표면세포인자수체IL-22R、IL-17R화IFN-γR1적표체；검측IL-22、IL-17、IFN-γ이급IFN-γ여IL-22혹IL-17조합대PMC중적Ki-67표체화조망적영향；검측결핵성흉강적액(TPE)급기분별여항IL-22、IL-17、IFN-γ단항조합대PMC중적Ki-67표체적영향.결과 (1)결핵분지간균감염시PMC표면고표체IL-22R、IL-17R화IFN-γR1[PMC적양성비례분별위(86.2±2.9)％、(41.5±4.4)％화(64.9±5.8)％]；(2)IL-22、IL-17조Ki-67양성PMC세포백분수분별위(31.5±2.0)％、(26.1±2.4)％,고우배양기조적(14.6±0.7)％(q치분별위6.8화4.9,균P＜0.05)；IFN-γ조위(5.2±1.2)％,저우완전배양기조(q=5.0,P＜0.05)；이IFN-γ+IL-22조위(23.4±1.7)％,IFN-γ+ IL-17조위(21.8±3.8)％,균고우IFN-γ조(q치분별위7.3화6.7,균P＜0.05).단독가입TPE혹가입함유동형대조IgG적TPE조분별위(63±9)％、(63±11)％,균고우완전배양기조(q치분별위19.6화19.7,균P＜0.05)；TPE가입항IFN-γ단항지후위(82±4)％,고우TPE+ IgG조(q=7.5,P＜0.05);TPE가입항IL-22단항후위(34±3)％,저우TPE+ IgG조(q=11.8,P＜0.05)；TPE가항IL-17단항조위(58±5)％,여TPE+ IgG조차이무통계학의의(q=2.1,P ＞0.05).(3) IFN-γ조PMC조망솔위(19.3±1.1)％,고우완전배양기조(4.3±0.6)％(q=33.4,P ＜0.05)；IL-22、IL-17조조망솔분별위(3.8±0.6)％화(5.7±0.8)％,여완전배양기조차이무통계학의의(q치분별위1.3화3.0,균P＞0.05).IFN-γ+IL-22조조망솔위(6.5±0.7)％,IFN-γ+ IL-17조위(8.7±1.7)％,균저우IFN-γ조(q치분별위28.5화23.6,균P＜0.05).결론 IL-22화IL-17촉진PMC증식이불도치기조망,병차능역전IFN-γ대PMC증식적억제작용,이급역전IFN-γ대PMC조망적유도작용；결핵분지간균감염배경가촉진PMC증식,해효응가능여TPE중IL-22、IL-17화IFN-γ적종합작용유관.
    Objective To investigate the effects of different cytokines (IL-22,IL-17,IFN-γ) on proliferation and apoptosis of human pleural mesothelial cells (PMC) during Mycobacterium tuberculosis infection.Methods The expressions of IL-22R,IL-17R and IFN-γR1 on PMC purified from tuberculous pleural effusion (TPE) were determined by flow cytometry.The effects of one or more of IL-22,IL-17,and IFN-γ on Ki-67 expression and apoptosis of PMC were explored.Ki-67 expression of PMC under the conditions of the absence or presence of exogenous TPE and with a combination of control IgG,or anti-IL-22,-IL-17 or-IFN-γ mAbs were determined.Results (1) During Mycobacterium tuberculosis infection,IL-22R,IL-17R and IFN-γR1 were highly expressed on the surface of PMC [(86.2 ± 2.9)％,(41.5 ±4.4)％ and (64.9 ±5.8)％ respectively].(2) In group IL-22 + IL-17,the percentage of Ki-67+ PMC was(31.5 ±2.0)％ and (26.1 ± 2.4)％ respectively,which were both higher than that in the medium group [(14.6 ± 0.7) ％] (q =6.8 and 4.9,respectively,both P ＜ 0.05).In group IFN-γ,the percentage of Ki-67 + PMC was (5.2 ± 1.2) ％,which was lower than that in the medium group (q =5.0,P ＜ 0.05).In group IFN-γ + IL-22 and IFN-γ + IL-17,the percentages of Ki-67 + PMC were (23.4 ± 1.7)％ and (21.8±3.8)％ respectively,which were both higher than that in group IFN-γ (q =7.3 and 6.7,respectively,both P ＜ 0.05).In group TPE and TPE + IgG,the percentages of Ki-67 + PMC were (63 ±9) ％ and(63 ± 11)％ respectively,which were both higher than that in the medium group (q =19.6 and 19.7,respectively,both P ＜0.05).In group TPE + anti-IFN-γγ mAb,the percentage of Ki-67 + PMC was (82 ±4) ％,which was even higher than that in group TPE + IgG (q =7.5,P ＜ 0.05).In group TPE +anti-IL-22 mAb,the percentage of Ki-67 + PMC was (34 ± 3) ％,which was lower than that in group TPE +IgG (q =11.8,P ＜ 0.05).In group TPE + anti-IL-17 mAb,the percentage of Ki-67 + PMC was (58 ±5) ％,which showed no significant difference compared to that in group TPE + IgG (q =2.1,P ＞ 0.05).(3) The percentage of apoptotic PMC in group IFN-γ was(19.3 ± 1.1)％,which was higher than that in the medium group [(4.3 ± 0.6) ％] (q =33.4,P ＜ 0.05).The percentage of apoptotic PMC in group IL-22 + IL-17 was (3.8 ± 0.6) ％ and (5.7 ± 0.8) ％ respectively,which had no significant difference compared to that in the medium group (q =1.3 and 3.0,respectively,both P ＞ 0.05).The percentage of apoptotic PMC in group IFN-γ + IL-22 and IFN-γ + IL-17 were (6.5 ± 0.7) ％ and (8.7 ± 1.7) ％respectively,which were both lower than that in group IFN-γ (q =28.5 and 23.6,respectively,both P ＜0.05).Conclusion During Mycobacterium tuberculosis infection,IFN-γ inhibited PMC proliferation and contributed to apoptosis,while IL-22 and IL-17 promoted PMC proliferation without influencing PMC apoptosis and succeeded in reversing the effect induced by IFN-γ.
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