Characterization of proinflammatory cytokine production and CD14 expression by murine alveolar macrophage cell lines.
Characterization of proinflammatory cytokine production and CD14 expression by murine alveolar macrophage cell lines.
复制标题
鼠肺泡巨噬细胞系促炎细胞因子产生和 CD14 表达的表征。
DOI：
10.1007/s11626-997-0116-0
复制
发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Vermeulen,MW
中科院分区：
文献类型：
--
作者：
Ryan,LK;Golenbock,DT;Wu,J;Vermeulen,MW
肺泡巨噬细胞在肺防御中发挥核心作用，它产生的细胞因子有助于协调局部炎症反应。在脓毒症等病理条件下，细菌脂多糖内毒素可诱导肺泡巨噬细胞(AM)释放促炎细胞因子，包括肿瘤坏死因子-α、白介素1和白介素6。研究控制肺泡巨噬细胞细胞因子产生的机制可能会导致更好的治疗炎性肺损伤的方法。我们和其他人已经注意到肺泡巨噬细胞和腹膜巨噬细胞之间的显著差异，但大量的人或小鼠肺泡巨噬细胞很少用于详细的机制研究。我们已经获得了三个小鼠肺泡巨噬细胞系(AMJ2C8、AMJ2C11和AMJ2C20)，并开始研究它们对促炎刺激的细胞因子反应。我们测量了内毒素、干扰素-γ以及两者的组合对每一株细胞产生肿瘤坏死因子、白介素1β和白介素6的影响。我们还研究了这些细胞内毒素受体CD14的表达，并探讨了血清对其内毒素反应性的影响。我们在这里显示，所有三种细胞系的反应方式与原代小鼠肺泡巨噬细胞的反应方式相当。观察到的这些线条之间的差异可能反映了在初级肺泡巨噬细胞群体中发现的已记录的异质性。这些细胞系应该会扩大可供研究人员研究小鼠肺泡巨噬细胞反应调节的工具。
Alveolar macrophages, which play a central role in lung defense, produce cytokines that help orchestrate local inflammatory responses. In sepsis and other pathological conditions, bacterial lipopolysaccharide endotoxin can induce alveolar macrophages (AM) to release proinflammatory cytokines, including tumor necrosis factor-alpha, interleukin-1, and interleukin-6. Studying the mechanisms that control alveolar macrophage cytokine production may lead to better therapies for conditions involving inflammatory lung injury. We and others have noted significant differences between alveolar macrophages and peritoneal macrophages, but large numbers of human or murine alveolar macrophages are rarely available for detailed mechanistic studies. We have obtained three murine alveolar macrophage cell lines (AMJ2C8, AMJ2C11, and AMJ2C20) and have begun to characterize their cytokine responses to proinflammatory stimuli. We measured the effects of endotoxin, interferon gamma, and the combination of the two on production of tumor necrosis factor, interleukin-1 beta, and interleukin-6 in each line. We also studied the expression of the endotoxin receptor CD14 by these cells, and investigated the effect of serum on their endotoxin responsiveness. We show here that all three of the cell lines responded in a manner comparable to that of primary murine alveolar macrophages. Observed variations between these lines may reflect the documented heterogeneity seen in populations of primary alveolar macrophages. These cell lines should expand the repertoire of tools available to investigators studying regulation of murine alveolar macrophage responses.