IL-17与IL-23／IL-17免疫通路在溃疡性结肠炎发病中的作用研究  

Role of IL - 17 and IL - 23/IL - 17 Immune - regulatory Pathway in the Pathogenesis of Ulcerative Colitis

作　　者：邢鹭[1] 韩英[1] 王志红[1] 王继恒[1] 

机构地区：[1]北京军区总医院消化内科,北京100700

出　　处：《医学新知》2010年第6期538-541,534,共5页New Medicine

摘　　要：目的 观察溃疡性结肠炎（UC）组、感染性腹泻（ID）组及健康对照（HC）组外周血单个核细胞（PBMCs）分泌IL-23的水平,以及在IL-23刺激下IL-17、IFN-γ的表达.方法 分离并培养UC组（29例）、ID组（20例）、HC组（26例）的PBMCs;ELISA方法 检测细菌脂多糖（LPS）刺激前后各组培养的PBMCs上清中IL-23水平以及IL-23诱导PBMCs分泌IL-17和IFN-γ的水平.结果 UC及ID组PBMCs上清中IL-23水平分别为（9.984±5.567）pg/ml、（9.843±4.970）pg/ml,明显高于HC组（4.295±5.181）pg/ml（P＜0.05）;LPS促进各组PBMCs分泌IL-23,UC组（146.627±86.199）pg/ml及ID组（149.852±51.418）pg/ml,明显高于HC组（72.222±51.863）pg/ml（P＜0.05）,而UC与ID组间比较无统计学意义;IL-23促进各组PBMCs分泌IL-17,UC组（63.631±11.793）pg/ml明显高于ID组（27.868±8.314）pg/ml及HC组（26.533±6.422）ps/ml,（P＜0.05）;IL-23促进各组PBMCs分泌IFN-γ,UC组（74.573±28.270）pg/ml及ID组（73.064±36.465）pg/ml显著高于HC组（5.167±3.701）pg/ml（P〈.05）,而UC与ID组间比较差别无统计学意义（P＞0.05）.结论 IL-23刺激是UC及ID发病的共同启动因素;IL-17分泌增多在UC的发病过程中发挥关键作用;IL-23/IL-17免疫通路调控异常是导致UC发病的重要机制.Objective To measure the expression of IL- 23 produced by peripheral blood mononuclear cells （PBMCs） in ulcerative colitis （UC） patients, inflammatory diarrhea （ID） and healthy controls （HC） and to analyze the effects of lipopolysaccharide（LPS） as well as IL - 23 on production of IL - 17 and IFN - γ. Methods PBMCs was isolated from 29 cases of UC ,20 cases of ID and 26 HC. IL -23 expressions were measured before and after the stimulation of LPS and IL - 17, IFN - γ expressions stimulated by IL - 23 were analyzed by ELISA. Results IL - 23 expressions in supernatants of cultured PBMCs of UC and ID groups were （9.984 ±5. 567 ）pg/ml and （9.843 ± 4. 970 ） pg/ml respectively, which were significantly higher than that of HC （4. 295 ± 5.181 ）pg/ml （P 〈 0.05 ）. LPS stimulated the production of IL - 23 for all groups and that of UC （ 146.627 ＋ 86. 199 ） pg/ml and ID （ 149. 852 ＋ 51. 418 ） pg/ ml were significantly higher than that of HC （ 72. 222 ± 51. 863 ） pg/ml （ P 〈 O. 05 ）, but no statistics was noticed between UC and ID. IL -23 stimulated the overproduction of IL - 17 by PBMCs in all groups, and that of UC（63. 631 ± 11. 793 ） pg/ml was much higher than that of ID （ 27. 868 ±8. 314 ） pg/ml and HC （ 26. 533 ± 6. 422 ） pg/ml （ P 〈 0.05 ）. IL - 23 also stimulated the production of IFN - γ by PBMCs of all groups, and that of UC （74.573± 28. 270） pg/ml and ID （73. 064 ± 36. 465 ）pg/ml were significantly higher than that of HC （ 5. 167 ± 3. 701 ）pg/ml （P 〈 0.05 ）, but no statistics was noticed between UC and ID. Conelusion IL - 23 might be the co - initiator of both UC and ID. IL - 17. plays a critical role in the development of UC. Impaired IL - 23/IL - 17 pathway might be involved in the pathogenesis of UC.

关 键 词：IIL-17 IL-23 Γ干扰素 溃疡性结肠炎 

分 类 号：R574.62[医药卫生—消化系统]