Kunkel S L, Chensue S W, Plewa M, Higashi G I
Am J Pathol. 1984 Feb;114(2):240-9.
The ability of arachidonic acid (AA) metabolites to regulate I-region-associated (Ia) antigen expression on macrophages from schistosome-egg-induced pulmonary granulomas was examined. The prostaglandin (PG) analog 15-S-15-CH3-PGE1 (M-PGE1) and PGF2 alpha were found to modulate the kinetics of Ia expression when administered in vivo. Methyl-PGE1 significantly suppressed Ia antigen expression by hypersensitivity granuloma macrophages, while PGF2 alpha appeared to potentiate the expression. Lymphokine-induced Ia antigen expression by cultured granuloma macrophages was likewise dramatically inhibited by M-PGE1. Further analysis using systemically administered inhibitors of AA metabolism demonstrated that the cyclooxygenase inhibitor indomethacin caused augmentation of Ia expression. In contrast, lipoxygenase inhibitors significantly reduced both Ia expression and granuloma size. The role of AA metabolites in modulating chronic inflammation is discussed.
研究了花生四烯酸（AA）代谢产物对血吸虫卵诱导的肺肉芽肿巨噬细胞上I区相关（Ia）抗原表达的调节能力。发现前列腺素（PG）类似物15-S-15-CH3-PGE1（M-PGE1）和PGF2α在体内给药时可调节Ia表达的动力学。甲基-PGE1显著抑制超敏反应性肉芽肿巨噬细胞的Ia抗原表达，而PGF2α似乎增强了表达。培养的肉芽肿巨噬细胞经淋巴因子诱导的Ia抗原表达同样被M-PGE1显著抑制。使用全身给药的AA代谢抑制剂进行的进一步分析表明，环氧合酶抑制剂吲哚美辛导致Ia表达增加。相反，脂氧合酶抑制剂显著降低了Ia表达和肉芽肿大小。讨论了AA代谢产物在调节慢性炎症中的作用。
