INFLUENCE OF STEROIDAL AND NONSTEROIDAL SEX-HORMONES ON HOST-RESISTANCE IN MICE - INCREASED SUSCEPTIBILITY TO LISTERIA-MONOCYTOGENES AFTER EXPOSURE TO ESTROGENIC HORMONES

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 the little estrogen activity, including 5.alpha.-dihydrotestosterone, progesterone, zearalenol and corticosterone, did not alter Listeria-related mortality. Estrogen-induced alterations in resistance were inhibited by adult thymectomy and by 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. Thus 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.