PROBLEM: Female sex hormones modulate a variety of humoral and cell-mediated immunologic functions. In this study, the effects of estrogen, progesterone, and testosterone on the chemiluminescence (CL) response and phagocytic ability of male rat peritoneal macrophages (M luminal diameter) were examined. METHOD: In M luminal diameter pretreated with 10(-2) ng/ml of 17 beta-estradiol (E2) for 20 hours, the CL generated in response to phorbol myristate acetate (PMA), 1,2-dioctanoyl-rac-glycerol (C8:0), or opsonized zymosan (OZ) was significantly increased by 135%, 140%, and 136% of control values, respectively. In addition, M luminal diameter treated with 10(-5) ng/ml or 10 ng/ml of E2 exhibited a significantly greater PMA- or OZ-stimulated CL response than did untreated controls. RESULTS: At 10(-2) ng/ml, progesterone enhanced and testosterone reduced the CL response, but these changes were not statistically significant. In time course studies, the PMA-stimulated CL response of M luminal diameter treated with 10(-2) ng/ml of E2 or progesterone for 5 h was significantly less than that of the untreated group. In the presence of endotoxin (12 pg/ml), the CL response in M luminal diameter treated with E2 or testosterone was significantly depressed as compared to untreated controls. Phagocytosis of opsonized sheep erythrocytes also was significantly enhanced (140% to 190% of control) when M luminal diameter were pretreated with 10(-12) M to 10(-8) M of either E2 or progesterone. CONCLUSIONS: These findings suggest that, at physiological concentrations, E2 is capable of modulating both CL generation and phagocytic uptake by M luminal diameter in a manner not shared by other steroid hormones.
PROBLEM: Female sex hormones modulate a variety of humoral and cell-mediated immunologic functions. In this study, the effects of estrogen, progesterone, and testosterone on the chemiluminescence (CL) response and phagocytic ability of male rat peritoneal macrophages (M luminal diameter) were examined. METHOD: In M luminal diameter pretreated with 10(-2) ng/ml of 17 beta-estradiol (E2) for 20 hours, the CL generated in response to phorbol myristate acetate (PMA), 1,2-dioctanoyl-rac-glycerol (C8:0), or opsonized zymosan (OZ) was significantly increased by 135%, 140%, and 136% of control values, respectively. In addition, M luminal diameter treated with 10(-5) ng/ml or 10 ng/ml of E2 exhibited a significantly greater PMA- or OZ-stimulated CL response than did untreated controls. RESULTS: At 10(-2) ng/ml, progesterone enhanced and testosterone reduced the CL response, but these changes were not statistically significant. In time course studies, the PMA-stimulated CL response of M luminal diameter treated with 10(-2) ng/ml of E2 or progesterone for 5 h was significantly less than that of the untreated group. In the presence of endotoxin (12 pg/ml), the CL response in M luminal diameter treated with E2 or testosterone was significantly depressed as compared to untreated controls. Phagocytosis of opsonized sheep erythrocytes also was significantly enhanced (140% to 190% of control) when M luminal diameter were pretreated with 10(-12) M to 10(-8) M of either E2 or progesterone. CONCLUSIONS: These findings suggest that, at physiological concentrations, E2 is capable of modulating both CL generation and phagocytic uptake by M luminal diameter in a manner not shared by other steroid hormones.
Authors: Brittney R Starling; Parag Kumar; Andrew T Lucas; David Barrow; Laura Farnan; Laura Hendrix; Hugh Giovinazzo; Gina Song; Paola Gehrig; Jeannette T Bensen; William C Zamboni Journal: Cancer Chemother Pharmacol Date: 2018-10-16 Impact factor: 3.333