Callis A H, Sohnle P G, Mandel G S, Mandel N S
Environ Res. 1986 Aug;40(2):301-12. doi: 10.1016/s0013-9351(86)80105-0.
The role of the complement system in the pathogenesis of crystal-induced pulmonary inflammation and fibrosis was evaluated using a mouse model of silicosis and congenitally complement-deficient mice. Mice lacking the fifth component of complement (B10.D2/o) were compared to C5-sufficient animals (B10.D2/n) for pulmonary changes following intratracheal instillation of silica crystals. Complement-deficient mice demonstrated a significant reduction compared to complement-sufficient mice in both cell number and protein content of lung lavage fluid throughout the 12 weeks following silica exposure. Lung hydroxyproline content (indicative of collagen deposition) was equivalent for both strains and significantly higher than controls at all time points following silica instillation. Moreover, studies in vitro have shown that silica crystals are capable of activating complement via the alternative pathway. These studies indicate that the complement system may be responsible for some of the pulmonary inflammation, but not fibrosis elicited by silica exposure.
利用矽肺小鼠模型和先天性补体缺陷小鼠，评估了补体系统在晶体诱导的肺部炎症和纤维化发病机制中的作用。将缺乏补体第五成分的小鼠（B10.D2/o）与补体充足的动物（B10.D2/n）进行比较，观察气管内注入二氧化硅晶体后肺部的变化。在二氧化硅暴露后的12周内，与补体充足的小鼠相比，补体缺陷小鼠肺灌洗液中的细胞数量和蛋白质含量均显著降低。两种品系的肺羟脯氨酸含量（指示胶原蛋白沉积）相当，且在注入二氧化硅后的所有时间点均显著高于对照组。此外，体外研究表明，二氧化硅晶体能够通过替代途径激活补体。这些研究表明，补体系统可能是二氧化硅暴露引发的部分肺部炎症的原因，但不是纤维化的原因。
