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Estrogens and Chlamydia trachomatis.

B Sugarman, P Agbor

    Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)
    |October 1, 1986
    PubMed
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    Estrogen, specifically 17-beta-estradiol, significantly increases Chlamydia trachomatis McCoy cell infections. This effect is dose-dependent and occurs without altering cell morphology, suggesting a non-structural mechanism of host susceptibility modification.

    Area of Science:

    • Reproductive Biology
    • Microbiology
    • Cell Biology

    Background:

    • Chlamydia trachomatis is a significant human pathogen.
    • McCoy cells are a common model for studying Chlamydia infections.
    • Hormonal influences on host-pathogen interactions are not fully understood.

    Purpose of the Study:

    • To investigate the effect of various hormones on Chlamydia trachomatis infection in McCoy cells.
    • To determine the specific role of estrogens in modulating Chlamydia infectivity.

    Main Methods:

    • Inoculation of nonreplicating McCoy cells with Chlamydia trachomatis.
    • Incubation with varying concentrations of hormones, particularly estrogens.
    • Assessment of Chlamydia binding and inclusion formation.

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  • Microscopic examination (light and electron) of McCoy cells.

    • Main Results:

    • 17-beta-estradiol significantly increased Chlamydia inclusions by approximately twofold.
    • The estrogen effect was dose-dependent and blocked by anti-estrogens.
    • No changes in initial Chlamydia binding or McCoy cell morphology were observed.
    • The effect was consistent in both replicating and nonreplicating McCoy cells.

    Conclusions:

    • Estrogens enhance Chlamydia trachomatis infectivity in McCoy cells.
    • This enhancement appears to be independent of morphological changes in host cells.
    • Estrogens may alter host cell susceptibility through non-structural mechanisms, impacting Chlamydia infections.