首都医科大学学报 ›› 2006, Vol. 27 ›› Issue (1): 32-34.

• 专题报道 • 上一篇    下一篇

IL-12、IL-18和TNF-α在外源性过敏性肺泡炎发病中的作用

童朝辉1, 陈宝敏1, 王辰1, Guzman Josune2, Costabel Ulrich2   

  1. 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, UniversityofEssen, 45239Essen, Germany
  • 收稿日期:2005-12-16 修回日期:1900-01-01 出版日期:2006-02-24 发布日期:2006-02-24

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

Tong Zhaohui1, Chen Baomin1, Wang Chen1, Guzman Josune2, Costabel Ulrich2   

  1. 1. Beijing Chaoyang Hospital, Beijing Institute of Respiratory Medicine, Capital University ofMedical Sciences;2. Ruhrlandklinik, University of Essen, 45239 Essen Germany
  • Received:2005-12-16 Revised:1900-01-01 Online:2006-02-24 Published:2006-02-24

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/L L-谷氨酰胺、200 kU/L青霉素及200 mg/L链霉素) 为培养液,加或不加内毒素(LPS,100 μg/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.

关键词: 外源性过敏性肺泡炎, 肺泡巨噬细胞, 细胞因子

Abstract: 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,100 μg/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 compared with controls(P<0.05 or P<0.01).Although the spontaneous 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.

Key words: extrinsic allergic alveolitis, alveolar macrophages, cytokine production

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