Influence of steroidal and nonsteroidal sex hormones on host resistance in mice: increased susceptibility to Listeria monocytogenes after exposure to estrogenic hormones

Abstract

Subchronic exposure to pharmacological levels of estrogenic compounds, including 1713-estradiol, diethylstilbestrol, and a-dienestrol, significantly increased the mortality of B6C3F, female mice after Listeria infection. Compounds with little estrogenic activity, including 5a-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 estrogenexposed mice to eliminate Listeria cells or to accumulate mononuclear effector cells at infective foci at the same rate as controls.

Scientific Opinion on the risks for public health related to the presence of zearalenone in food

“…As reported by JECFA (FAO/WHO, 2000), the in vivo immunotoxicity of zearalenone was investigated in mice receiving zearalenone by subcutaneously (s.c.) (Pung et al, 1984) or oral administration (Forsell et al, 1986;Pestka et al, 1987). In these studies, zearalenone did not affect either the sensitivity to Listeria monocytogenes infection, the serum immunoglobulins concentration or the leucocyte cell count in blood.…”

Female Sex Hormones Modulate the Function of LPS‐treated Macrophages

“…Treatment of male and female mice infected with Toxoplasma gondii or Listeria monocytogenes with E 2 or estrogenic compounds increased host mortality, while ovariectomy or orchiectomy increased resistance to the infection. 16,17 Pharmacological doses of estrogen increase sensitivity of hepatic macrophages (Kupffer cells) to endotoxin and enhance endotoxininduced mortality in rats. 18,19 In contrast, estrogen treated mice or rats are less susceptible to endotoxin (lipopolysaccharide, LPS) 20,21 or to infection with bacteria such as Pneumococcus type I, Pasteurella septica, and Salmonella typhimurium.…”

Hormonal modulation of sex differences in resistance to Leishmania major systemic infections

“…Sex-associated differences in patterns of resistance to bacterial, viral, and parasitic infection (10,12,15,20,32,36,40), tumor development (4), autoimmune responses (1; A. H. W. Schuurs, Clin. Immunol.…”