Dixon Dani-Louise, Barr Heather A, Bersten Andrew D, Doyle Ian R
Department of Critical Care Medicine, Flinders University, Adelaide, SA 5006, Australia.
Exp Lung Res. 2008 Jan;34(1):37-47. doi: 10.1080/01902140701807928.
Cell stretch stimulates both surfactant and cytokine production. The authors proposed that stretch, through these effects, modifies the pathogenesis of lipopolysaccharide-induced acute lung injury (ALI), and that this is CO(2) dependent. Rat alveolar type II cells and macrophages were co-cultured with lipopolysaccharide in 5%, 10%, or 20% CO(2) +/- stretch (30%, 60 cycles/min) for 6 hours. Intracellular TNF-alpha and IL-6 increased whereas secreted cytokine and surfactant decreased with increasing CO(2). Stretch independently increased intracellular TNF-alpha and decreased IL-6 secretion. Elevated CO(2) may therefore diminish secretion of proinflammatory cytokines by alveolar cells, contributing to an explanation for protective hypercapnia in ALI.
细胞拉伸可刺激表面活性剂和细胞因子的产生。作者提出，通过这些作用，拉伸可改变脂多糖诱导的急性肺损伤（ALI）的发病机制，且这一过程依赖于二氧化碳。将大鼠肺泡Ⅱ型细胞和巨噬细胞与脂多糖在5%、10%或20%二氧化碳环境中共同培养，并施加或不施加拉伸（30%，60次/分钟），持续6小时。随着二氧化碳浓度升高，细胞内肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）增加，而分泌的细胞因子和表面活性剂减少。拉伸可独立增加细胞内TNF-α并减少IL-6分泌。因此，二氧化碳升高可能会减少肺泡细胞促炎细胞因子的分泌，这有助于解释ALI中保护性高碳酸血症的现象。
