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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 To evaluate the effects of interleukin-12 (IL-12), interleukin-18 (IL-18) and tumor necrosis factor-α (TNF- α) in alveolar macrophages (AM) The role of extrinsic allergic alveolitis (EAA) in inflammation and pathogenesis. Methods Eleven patients with EAA and 10 normal controls were enrolled in this study. AM with 10% RPMI (containing 10% heat inactivated fetal bovine serum, 2 mmol / L L-glutamine, 200 kU / L penicillin and 200 mg / ) Were cultured with or without endotoxin (LPS, 100μg / L) AM for 24 h. The cytokine content in culture supernatants was determined by ELISA. Results Compared with the control group, the levels of IL-18 and TNF-α were significantly increased in EAA patients (P <0.05 or P <0.01), with or without endotoxin stimulation. The level of spontaneous release of IL-12 in EAA patients was very low, and was significantly increased after endotoxin stimulation (P <0.01). Conclusion IL-12, IL-18 and TNF-α may play an important role in the pathogenesis of EAA inflammation and granuloma formation.