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目的 探讨肺血管内巨噬细胞 (PIM)释放的细胞因子在感染性急性肺损伤 (ALI)发病中的作用。方法 仿Morton法灌洗肺血管床 ,贴壁法分离猪PIM ,培养于RPMI 16 40培养基 ,予 10 μg/ml脂多糖 (LPS)刺激 ,胸腺细胞增殖法测PIM培养上清白细胞介素 1β(IL - 1β)活性 ,酶联免疫吸附试验 (ELISA)法测肿瘤坏死因子α(TNFα)、白细胞介素 6 (IL - 6 )、白细胞介素 8(IL - 8)含量。结果 LPS刺激后 ,PIM释放TNFα、IL - 1β和IL - 6均呈单峰样显著增加 ,峰值分别出现在刺激后的 1h、2h和 4h(P <0 0 1) ;而IL - 8则于刺激后的 4～ 8h持续升高 (P <0 0 5～ 0 0 1)。结论 LPS刺激后 ,PIM分泌多种细胞因子 ,其中TNFα、IL - 1β升高最早 ,提示其在ALI的发生中起重要作用 ;而IL - 6、IL - 8升高较晚 ,且后者持续时间长 ,可能对ALI的病情进展起重要作用。细胞因子间的相互作用在ALI的发病中似更重要
Objective To investigate the role of cytokines released by pulmonary vascular macrophages (PIMs) in the pathogenesis of infectious acute lung injury (ALI). Methods Pulmonary vascular beds were perforated by morton method and porcine PIMs were isolated by adherent method. The cells were cultured in RPMI 1640 medium and stimulated with lipopolysaccharide (LPS) at 10 μg / ml. The supernatants of PIM supernatants were measured by thymocyte proliferation assay. The levels of IL - 1β, IL - 6 and IL - 8 were measured by enzyme - linked immunosorbent assay (ELISA). Results After LPS stimulation, the levels of TNFα, IL - 1β and IL - 6 released by PIM significantly increased in unimodal, peaked at 1h, 2h and 4h after stimulation (P <0.01) After 4 ~ 8h stimulation continued to increase (P <0 0 5 ~ 0 0 1). Conclusions After LPS stimulation, PIMs secrete a variety of cytokines, of which TNFα and IL - 1β are the first to be elevated, suggesting that PIM plays an important role in the pathogenesis of ALI. IL - 6 and IL - 8 rise later, and the latter continues A long time may play an important role in the progression of ALI. The interaction between cytokines appears to be more important in the pathogenesis of ALI