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肺表面活性物质蛋白A刺激肺泡巨噬细胞的趋化作用。

Pulmonary surfactant protein A stimulates chemotaxis of alveolar macrophage.

作者信息

Wright J R, Youmans D C

机构信息

Cardiovascular Research Institute, University of California, San Francisco 94143.

出版信息

Am J Physiol. 1993 Apr;264(4 Pt 1):L338-44. doi: 10.1152/ajplung.1993.264.4.L338.

Abstract

Pulmonary surfactant modulates several functions of alveolar macrophages including phagocytosis, killing, and chemotaxis. We hypothesized that the reported stimulatory effect of surfactant on macrophage migration was mediated by one of the surfactant proteins, SP-A. We found that macrophage migration was stimulated by SP-A in a concentration-dependent manner. A concentration of 105 micrograms SP-A/ml enhanced migration approximately 10-fold. Heat treatment or reduction and alkylation of SP-A reduced its stimulatory effect. A checker-board analysis showed that SP-A stimulated migration primarily by enhancing chemotaxis (directed movement) rather than chemokinesis (random movement). The interaction of SP-A with macrophages may be mediated at least partly by the collagen-like domain of SP-A. We speculate that SP-A may play a multifunctional role in regulating pulmonary immune response by stimulating multiple macrophage functions.

摘要

肺表面活性物质可调节肺泡巨噬细胞的多种功能,包括吞噬作用、杀伤作用和趋化作用。我们推测,表面活性物质对巨噬细胞迁移的刺激作用是由表面活性蛋白之一SP-A介导的。我们发现,SP-A以浓度依赖性方式刺激巨噬细胞迁移。105微克SP-A/毫升的浓度可使迁移增强约10倍。对SP-A进行热处理或还原及烷基化处理会降低其刺激作用。棋盘分析表明,SP-A主要通过增强趋化作用(定向运动)而非趋化活性(随机运动)来刺激迁移。SP-A与巨噬细胞的相互作用可能至少部分由SP-A的胶原样结构域介导。我们推测,SP-A可能通过刺激多种巨噬细胞功能在调节肺部免疫反应中发挥多功能作用。

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