De Krey G K, Baecher-Steppan L, Fowles J R, Kerkvliet N I
Department of Agricultural Chemistry, Oregon State University, Corvallis 97331.
Toxicol Lett. 1994 Dec;74(3):211-20. doi: 10.1016/0378-4274(94)90080-9.
Prostaglandin-E2 (PGE2) was investigated for its role in suppression of splenic cytotoxic T lymphocyte (CTL) activity following exposure to 3,3',4,4',5,5'-hexachlorobiphenyl (HxCB) in mice. Following i.p. alloantigen injection, PGE2 levels significantly increased in peritoneal fluid and in spleen cell culture supernatants. HxCB exposure (1) significantly elevated PGE2 levels above control in peritoneal fluid, (2) significantly reduced production of PGE2 by spleen cells, and (3) did not alter PGE2 production by peritoneal cells. The levels of PGE2 observed were below (> 100-fold) those shown by others to cause immune suppression, and splenic CTL activity was unaltered by indomethacine treatment sufficient to reduce peritoneal PGE2 to undetectable levels. We conclude that altered PGE2 production is not involved in suppression of CTL activity by HxCB.
研究了前列腺素 - E2（PGE2）在小鼠接触3,3',4,4',5,5'-六氯联苯（HxCB）后对脾细胞毒性T淋巴细胞（CTL）活性抑制中的作用。腹腔注射同种异体抗原后，腹腔液和脾细胞培养上清液中的PGE2水平显著升高。HxCB暴露（1）使腹腔液中PGE2水平显著高于对照，（2）显著降低脾细胞产生PGE2的量，（3）未改变腹腔细胞产生PGE2的情况。观察到的PGE2水平低于（>100倍）其他研究显示可引起免疫抑制的水平，并且用消炎痛处理足以将腹腔PGE2降低到无法检测的水平，但脾细胞毒性T淋巴细胞活性未改变。我们得出结论，PGE2产生的改变不参与HxCB对细胞毒性T淋巴细胞活性的抑制。
