Inhibition of human polymorphonuclear cell oxidative burst by 17-β-estradiol and 2,3,7,8-tetrachlorodibenzo-p-dioxin

被引:13
作者
Abrahams, VM [1 ]
Collins, JE [1 ]
Wira, CR [1 ]
Fanger, MW [1 ]
Yeaman, GR [1 ]
机构
[1] Dartmouth Coll Sch Med, Dept Microbiol & Immunol, Lebanon, NH 03756 USA
来源
AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY | 2003年 / 50卷 / 06期
关键词
aryl hydrocarbon receptor; estrogen receptor; neutrophil; superoxide; TCDD;
D O I
10.1046/j.8755-8920.2003.00111.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
PROBLEM: Polymorphonuclear cell (PMN) function may be directly influenced by 17-beta-estradiol and the endocrine disruptor, 2,3,7,8-tetrachloro-dibenzo-p-dioxin (TCDD). This may have significant consequences on PMN function within the female reproductive tract. This study evaluated the effects of 17-beta-estradiol and TCDD on PMN oxidative burst. METHOD OF STUDY: Peripheral blood PMN were isolated from normal male donors. Following treatment with 17-beta-estradiol, TCDD or both, PMN were stimulated with phorbol 12-myristate 13-acetate. Superoxide production was measured by lucigenin-enhanced chemiluminescence. RESULTS: Following 24-hr culture with either 17-beta-estradiol or TCDD, PMN superoxide production was significantly reduced, however, no such inhibition was observed when PMN were cultured with both estradiol and TCDD. Using antagonists the estradiol and, TCDD effects on PMN superoxide production was shown to be estrogen and aryl hydrocarbon receptor mediated. CONCLUSIONS: Estradiol and TCDD influence PMN oxidative burst through receptor mediated events. Such altered PMN function may have profound effects upon the normal endometrial cycle.
引用
收藏
页码:463 / 472
页数:10
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