Surfactant protein A differentially regulates IFN-gamma- and LPS-induced nitrite production by rat alveolar macrophages.

Surfactant protein A differentially regulates IFN-gamma- and LPS-induced nitrite production by rat alveolar macrophages.
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表面活性剂蛋白 A 差异性调节大鼠肺泡巨噬细胞的 IFN-γ 和 LPS 诱导的亚硝酸盐产生。

DOI:
10.1165/ajrcmb.23.6.4083
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发表时间:
2000
期刊:
American journal of respiratory cell and molecular biology.
影响因子:
--
通讯作者:
Wright,JR
Wright,JR
中科院分区:
--
文献类型:
--
作者:
Stamme,C;Walsh,E;Wright,JR

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尽管一些研究表明肺表面活性物质蛋白(SP)-A和SP-D通过增强病原体吞噬功能而参与天然免疫,但SP-A和SP-D在调节自由基和细胞因子的产生中的作用仍存在争议。我们推测免疫细胞的激活状态和机制影响其对SP-A的反应。采用体外培养的大鼠肺泡巨噬细胞,观察SP-A和SP-D对脂多糖、干扰素-γ或两者同时激活的大鼠肺泡巨噬细胞产生一氧化氮和诱导型一氧化氮合酶的影响。SP-A抑制光滑内毒素刺激的巨噬细胞产生NO和iNOS,但不能明显结合SP-A,而粗脂多糖则能强烈结合SP-A。相反,SP-A可促进干扰素-γ或干扰素-γ+脂多糖刺激的细胞产生NO和iNOS。SP-A和SP-D均不影响基线NO的产生,SP-D对脂多糖或干扰素-γ刺激的细胞产生NO也没有显著影响。这些结果表明,SP-A通过对免疫细胞的激活状态和机制的不同而对免疫细胞的反应产生不同的影响,从而参与了肺炎性反应。
Although several studies have demonstrated that the pulmonary collectins surfactant protein (SP)-A and SP-D contribute to innate immunity by enhancing pathogen phagocytosis, the role of SP-A and SP-D in regulating production of free radicals and cytokines is controversial. We hypothesized that the state and mechanism of activation of the immune cell influence its response to SP-A. The effects of SP-A and SP-D on production of nitric oxide (NO) and inducible nitric oxide synthase (iNOS) were assessed in isolated rat alveolar macrophages activated with lipopolysaccharide (LPS), interferon gamma (IFN- γ ), or both agonists. SP-A inhibited production of NO and iNOS in macrophages stimulated with smooth LPS, which did not significantly bind SP-A, or rough LPS, which avidly bound SP-A. In contrast, SP-A enhanced production of NO and iNOS in cells stimulated with IFN- γ or INF- γ plus LPS. Neither SP-A nor SP-D affected baseline NO production, and SP-D did not significantly affect production of NO in cells stimulated with either LPS or IFN- γ . These results suggest that SP-A contributes to the lung inflammatory response by exerting differential effects on the responses of immune cells, depending on their state and mechanism of activation.