Hii Charles S, Ferrante Antonio
Department of Immunopathology, Children, Youth and Women's Health Services, 72 King William Road, North Adelaide, South Australia 5006, Australia.
Arch Immunol Ther Exp (Warsz). 2007 Mar-Apr;55(2):99-110. doi: 10.1007/s00005-007-0014-x. Epub 2007 Mar 20.
Arachidonic acid (AA), a second-messenger molecule released from membrane phospholipids by phospholipase A(2) in activated cells, is a stimulator of neutrophil responses, including the oxygen-dependent respiratory burst. The polyunsaturated fatty acid is also the precursor of biologically active eicosanoids. There are several mechanisms by which AA stimulates the respiratory burst. These include the direct binding of AA to S100 proteins which regulate the assembly of the NADPH oxidase as well as the activation of key signaling molecules which control the respiratory burst. Arachidonic acid also stimulates it own release from membrane phospholipids and this contributes to optimal respiratory burst activity. Thus, increased levels of AA at sites of inflammation will influence the magnitude and course of the inflammatory response, not only by directly affecting the function of infiltrating neutrophils and other leukocytes, but also through its metabolites generated by lipoxygenases and cyclooxygenases.
花生四烯酸（AA）是一种在活化细胞中由磷脂酶A2从膜磷脂释放的第二信使分子，是中性粒细胞反应的刺激物，包括氧依赖性呼吸爆发。这种多不饱和脂肪酸也是生物活性类二十烷酸的前体。花生四烯酸通过多种机制刺激呼吸爆发。这些机制包括花生四烯酸直接与调节NADPH氧化酶组装的S100蛋白结合，以及激活控制呼吸爆发的关键信号分子。花生四烯酸还刺激其自身从膜磷脂中释放，这有助于最佳的呼吸爆发活性。因此，炎症部位花生四烯酸水平的升高将影响炎症反应的程度和进程，不仅通过直接影响浸润的中性粒细胞和其他白细胞的功能，还通过脂氧合酶和环氧化酶产生的代谢产物来实现。
