Sitrin R G, Kaltreider H B, Goldyne M E
J Immunol. 1984 Feb;132(2):867-71.
We demonstrated previously that rabbit alveolar macrophages stimulated in vitro by bacterial lipopolysaccharide (LPS) have markedly enhanced procoagulant activity (PCA), caused by increased production of a cell-associated tissue thromboplastin. The present study examined the role of arachidonic acid metabolites in modulating the expression of this PCA. Alveolar macrophages lavaged from normal rabbits were incubated in vitro with LPS, indomethacin, and purified prostaglandins, and the resultant PCA was measured. LPS stimulated a significant increase in macrophage PCA relative to unstimulated controls (p less than 0.01). Indomethacin suppressed the ability of LPS to stimulate PCA in a dose-related fashion. The addition of PGE2 or PGE1 reversed the suppressive action of indomethacin (p less than 0.01), whereas PGF2 alpha, PGD2, TXB2, and 6-keto PGF1 alpha had no such effect. PGE2 did not affect PCA unless the macrophages were also stimulated with LPS. A significant correlation (rs = 0.72, p less than 0.01) existed between the level of LPS-stimulated macrophage PCA and the corresponding amount of immunoreactive PGE2 released into the culture medium. The results of this study demonstrate that PGE is required for the LPS-mediated enhancement of rabbit alveolar macrophage-associated tissue thromboplastin and that PGE can stimulate the expression of PCA by appropriately conditioned cells.
我们先前已证明，经细菌脂多糖（LPS）体外刺激的兔肺泡巨噬细胞具有显著增强的促凝血活性（PCA），这是由细胞相关组织凝血活酶产量增加所致。本研究检测了花生四烯酸代谢产物在调节这种PCA表达中的作用。将从正常兔灌洗得到的肺泡巨噬细胞与LPS、吲哚美辛和纯化的前列腺素在体外孵育，并测定产生的PCA。与未刺激的对照相比，LPS刺激巨噬细胞PCA显著增加（p小于0.01）。吲哚美辛以剂量相关的方式抑制LPS刺激PCA的能力。添加PGE2或PGE1可逆转吲哚美辛的抑制作用（p小于0.01），而PGF2α、PGD2、TXB2和6-酮-PGF1α则无此作用。除非巨噬细胞也用LPS刺激，否则PGE2不会影响PCA。LPS刺激的巨噬细胞PCA水平与释放到培养基中的相应免疫反应性PGE2量之间存在显著相关性（rs = 0.72，p小于0.01）。本研究结果表明，PGE是LPS介导的兔肺泡巨噬细胞相关组织凝血活酶增强所必需的，并且PGE可通过适当预处理的细胞刺激PCA的表达。
