IL-12I、L-18和TNF-α在外源性过敏性肺泡炎发病中的作用  

Production of IL-12,IL-18 and TNF-α by Alveolar Macrophages in Extrinsic Allergic Alveolitis

作　　者：童朝辉[1] 陈宝敏 王辰[3] Guzman Josune Costabel Ulrich 

机构地区：[1]首都医科大学附属北京朝阳医院北京呼吸疾病研究所 [2]Ruhrlandklinik University of Essen,essengermany45239 [3]首都医科大学附属北京朝阳医院

出　　处：《首都医科大学学报》2006年第1期32-34,共3页Journal of Capital Medical University

基　　金：首都医学发展科研基金(首都ZD199901)资助项目

摘　　要：目的从临床的角度出发、评价肺泡巨噬细胞(alveolar macrophages,AM)的产物白介素-12(IL-12)、白介素-18(IL-18)和肿瘤坏死因子-α(TNF-α)在外源性过敏性肺泡炎(extrinsic allergic alveolitis,EAA)炎症形成及发病中的作用。方法收集11例EAA患者和10例正常对照的AM,以10%RPMI(含有10%热灭活胎牛血清、2 mmol/LL-谷氨酰胺、200 kU/L青霉素及200mg/L链霉素)为培养液,加或不加内毒素(LPS,100μg/L)进行AM培养24 h。用ELISA方法测定培养上清液中细胞因子含量。结果与对照组相比,无论有无内毒素刺激,IL-18和TNF-α的水平在EAA患者中均明显增加(P<0.05或P<0.01)。EAA患者自发释放的IL-12的水平很低,内毒素刺激后明显升高(P<0.01)。结论IL-12、IL-18和TNF-α可能参与EAA炎症和肉芽肿形成过程,在其发病中起重要作用。Objective This study was performed to evaluate the effect of the production of interleukin-12（IL-12）, interleukin- 18 （IL-18） and tumor necrosis factor-α（TNF-α） in the development and pathogenesis of Extrinsic allergic alveolitis（EAA）. Methods AM from 11 patients with EAA and 10 control subjects were cultured for 24 h in 10% RPMI medium alone, or with RPMI medium and lipopolysaccharide （LPS, 100μg/L）. Cytokines in the culture supernatants were assayed by ELISA. Results The production of IL- 18 and TNF-α was increased in patients with EAA in either absence or presence of LPS compareed with controls（ P 〈 0.05 or P〈 0.01）. Although the spontanocus production of IL-12 was low, with LPS stimulation it was significantly elevated in EAA（ P 〈 0.01 ）. Conclusion These observations suggest that IL-12, IL-18 and TNFα may be involved in the pathogenesis of EAA,

关 键 词：外源性过敏性肺泡炎 肺泡巨噬细胞 细胞因子 

分 类 号：R563.1[医药卫生—呼吸系统]