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Toxoplasma gondii: decreased resistance to infection in mice due to estrogen
Abstract:
Exposure to pharmacological concentrations of potent estrogenic compounds, including 17 beta-estradiol, diethylstilbestrol, and alpha-dienestrol, increased the susceptibility of mice to Toxoplasma gondii as measured by brain cyst formation. Compounds with weak estrogenic activity or other hormonal activity, including 5 alpha-dihydrotestosterone, progesterone, and zearalanol, did not alter host resistance to infection. The ability of estrogens to alter susceptibility was inhibited by the estrogen antagonist, tamoxifen. The restoration of ovariectomized mice with normal physiological concentrations of estrogen had no effect on subsequent infection with T. gondii. These results indicate that pharmacological, but not physiological, levels of estrogen selectively alter host resistance to T. gondii, possibly through hormonal events.
Insights
Pharmacological estrogen concentrations increase susceptibility to Toxoplasma gondii infection in mice. Physiological estrogen levels and other hormones do not affect host resistance, suggesting selective estrogenic effects.
Area of Science:
- Immunology
- Endocrinology
- Parasitology
Background:
- Estrogenic compounds are known to modulate immune responses.
- Toxoplasma gondii is an opportunistic parasite that establishes chronic infections.
- Understanding host-pathogen interactions is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the effect of estrogenic compounds on host susceptibility to Toxoplasma gondii infection.
- To determine if estrogen's effect is dose-dependent and selective for estrogenic activity.
- To explore the role of estrogen antagonists and physiological estrogen levels in modulating host resistance.
Main Methods:
- Mice were exposed to various estrogenic compounds at pharmacological or physiological concentrations.
- Host susceptibility was assessed by measuring brain cyst formation after T. gondii infection.
- The effects of estrogen antagonists and other hormones were evaluated.
Main Results:
- Potent estrogenic compounds (17 beta-estradiol, diethylstilbestrol, alpha-dienestrol) at pharmacological doses increased susceptibility to T. gondii.
- Weakly estrogenic compounds (5 alpha-dihydrotestosterone, progesterone, zearalanol) did not alter host resistance.
- The estrogen antagonist tamoxifen inhibited the effect of estrogens on susceptibility.
- Physiological estrogen concentrations in ovariectomized mice did not affect T. gondii infection.
Conclusions:
- Pharmacological concentrations of potent estrogens, but not physiological levels or other hormones, selectively increase host susceptibility to T. gondii.
- Estrogen's modulation of host resistance to T. gondii appears to be mediated by specific hormonal events.
- These findings highlight the complex interplay between hormonal status and parasitic infections.