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pubmed:abstractText |
Subchronic exposure to pharmacological levels of estrogenic compounds, including 17 beta-estradiol, diethylstilbestrol, and alpha-dienestrol, significantly increased the mortality of B6C3F1 female mice after Listeria infection. Compounds with little estrogenic activity, including 5 alpha-dihydrotestosterone, progesterone, zearalenol, and corticosterone, did not alter Listeria-related mortality. Estrogen-induced alterations in resistance were inhibited by both adult thymectomy and the estrogen antagonist tamoxifen. Estrogen exposure depressed the accumulation of monocytes and lymphocytes at infective foci. Significantly elevated numbers of bacteria were observed in infective foci of estrogen-treated mice later in the infection when bacteria were nearly eliminated from untreated animals. These results indicate that estrogen-induced suppression of Listeria immunity is partially mediated by the thymus, probably through receptor events which may ultimately suppress the activation of T cell-dependent defense mechanisms. This may be partially reflected by the inability of estrogen-exposed mice to eliminate Listeria cells or to accumulate mononuclear effector cells at infective foci at the same rate as controls.
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