一氧化氮對巨噬細胞移行能力的影響

當細菌入侵時，會誘導巨噬細胞的活化，使之釋放大量NO參與免疫反應。本文研究發現，在RAW264.7巨噬細胞中，NO可誘發c-Src及Eps8蛋白表現量增加。另外，利用老鼠作為model，抽取的thioglycolate-elicited peritoneal macrophages（PEM）在NO刺激下，c-Src及Eps8蛋白表現量同樣呈現明顯增加的現象。此外，NO也會增加RAW264.7巨噬細胞及PEM細胞移行的能力。我們更進一步將SNAP（NO donor）注射至老鼠腹腔中，再抽取其巨噬細胞做研究，發現其c-Src、Eps8的蛋白量及細胞移行的能力都明顯增加，這和之前的結果不謀而合。由於PP2（Src kinase inhibitor）會抑制巨噬細胞的NO-induced migration，且表達eps8 siRNA的RAW264.7細胞喪失NO-induced migration的能力。因此，我們認為在NO誘導巨噬細胞移行的過程中，c-Src及Eps8扮演著重要角色。

During bacterial infections, macrophages are activated and release large amount of NO to perform a variety of cellular functions. In this study, NO could increased c-Src and Eps8 protein levels were observed in SNAP-treated RAW264.7 cells. And similar results were also demonstrated in thioglycolate-elicited peritoneal macrophages (PEM) exposed to SNAP. Moreover, elevated migration of RAW264.7 cells and PEM were detected in response to SNAP. Remarkably, macrophage recoverd from SNP-challenged mice not only exhibited enhanced c-Src and Eps8 expression, but also increased motility. Due to PP2（Src kinase inhibitor）can abolish SNAP-induced cell migration and reduced cellular movement was detected in SNAP exposure, we conclude that c-Src and Eps8 are NO-induced and play an important role in NO-induced macrophage migration.