SURFACTANT PROTEIN-A STIMULATION OF INFLAMMATORY CYTOKINE AND IMMUNOGLOBULIN PRODUCTION
SURFACTANT PROTEIN-A STIMULATION OF INFLAMMATORY CYTOKINE AND IMMUNOGLOBULIN PRODUCTION
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DOI：
10.1152/ajplung.1994.267.6.l712
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发表时间：
1994-12-01
影响因子：
4.9
通讯作者：
PHELPS, DS
中科院分区：
文献类型：
--
作者：
KREMLEV, SG;PHELPS, DS
肺表面活性物质在肺内起着多种与免疫功能调节有关的作用。在这方面特别感兴趣的是表面活性蛋白A（SP-A），一种钙依赖性凝集素。我们以前曾报道，SP-A增强刀豆球蛋白A诱导的增殖，在这项研究中，我们研究了肿瘤坏死因子-α（TNF-α），白细胞介素1 α，1 β，和6，和干扰素-γ的人外周血单核细胞的分泌。SP-A增加了除干扰素-γ外的所有细胞因子的水平。在大鼠外周血细胞、脾细胞和肺泡巨噬细胞中，我们发现SP-A对TNF-α的释放也有类似的增强作用。在SP-A和表面活性剂脂质的组合中，由SP-A处理引起的TNF-α水平的增加随着脂质的增加而降低。在较高的SP-A相对浓度下，脂质几乎没有或没有影响。SP-A还增强了大鼠脾细胞免疫球蛋白A、G和M的产生。每种同种型的水平都比对照水平增加了几倍。这些数据表明SP-A能够通过调节细胞因子产生和免疫球蛋白分泌来调节肺中的免疫细胞功能。
Pulmonary surfactant plays a variety of roles related to the regulation of immune function in the lung. Of particular interest in this regard is surfactant protein A (SP-A), a calcium-dependent lectin. We have reported previously that SP-A enhances concanavalin A-induced proliferation, and in this study we examined the secretion of tumor necrosis factor-alpha (TNF-alpha), interleukins 1 alpha, 1 beta, and 6, and interferon-gamma by human peripheral blood mononuclear cells. Levels of all of the cytokines except interferon-gamma were increased by SP-A. In rat peripheral blood cells, splenocytes, and alveolar macrophages we found a similar enhancement of TNF-alpha release by SP-A. In combinations of SP-A and surfactant lipids, the increased levels of TNF-alpha resulting from SP-A treatment decreased as the lipids increased. At higher relative concentrations of SP-A, the lipids had little or no effect. SP-A also enhanced the production of immunoglobulins A, G, and M by rat splenocytes. Levels of each isotype were increased severalfold over control levels. These data demonstrate that SP-A is capable of modulating immune cell function in the lung by regulating cytokine production and immunoglobulin secretion.