Rediske J J, Pickering R J
Cell Immunol. 1984 Oct 15;88(2):241-50. doi: 10.1016/0008-8749(84)90158-8.
The ability of exogenous prostaglandins to inhibit complement production (CP) by monocytes and macrophages (M phi) suggests that endogenous arachidonic acid metabolites produced by these cells may also regulate their rate of CP. We assessed the regulatory influence of endogenous metabolites on CP by M phi utilizing exogenous arachidonic acid and serum-opsonized zymosan as stimulators of production of cyclooxygenase and lipoxygenase metabolites. The results of this study show that (i) the inhibition of CP caused by both agents is is independent of arachidonic acid metabolites, suggesting that endogenously produced metabolites do not influence CP, and (ii) arachidonic acid and serum-opsonized zymosan inhibit production by independent mechanisms.
外源性前列腺素抑制单核细胞和巨噬细胞(M phi)补体生成(CP)的能力表明,这些细胞产生的内源性花生四烯酸代谢产物也可能调节其CP速率。我们通过使用外源性花生四烯酸和血清调理酵母聚糖作为环氧化酶和脂氧化酶代谢产物生成的刺激物,评估了内源性代谢产物对M phi的CP的调节影响。本研究结果表明:(i)两种试剂引起的CP抑制均与花生四烯酸代谢产物无关,提示内源性产生的代谢产物不影响CP;(ii)花生四烯酸和血清调理酵母聚糖通过独立机制抑制生成。