Título : |
Estrogens inhibit mycelium-to-yeast transformation in the fungus Paracoccidioides brasiliensis: Implications for resistance of females to Paracoccidioidomycosis |
Tipo de documento : |
documento electrónico |
Autores : |
Ángela Restrepo Moreno, ; Maria E. Salazar, ; Luz Elena Cano Restrepo, |
Fecha de publicación : |
1984 |
Títulos uniformes : |
Infection and Immunity
|
Idioma : |
Inglés (eng) |
Resumen : |
Evidence that disease due to the thermally dimorphic fungus Paracoccidioides brasiliensis occurs post-puberty predominantly in males led us to hypothesize that hormonal factors critically affect its pathogenesis. We show here that estrogens inhibit mycelial- to yeast-form transformation of P. brasiliensis in vitro. Transformation of three isolates was inhibited to 71, 33, and 19% of the control values in the presence of 10(-10), 10(-8), and 10(-6) M 17 beta-estradiol, respectively. The synthetic estrogen diethylstilbestrol was active but less potent than estradiol, whereas testosterone, 17 alpha-estradiol, tamoxifen, and corticosterone were inactive. This function was specifically inhibited, since yeast-to-mycelium transformation, yeast growth, and yeast reproduction by budding were unaffected by 17 beta-estradiol. Of note is the fact that mycelium-to-yeast transformation occurs as the first step in vivo in the establishment of infection. The cytosol of the three isolates studied possesses a steroid-binding protein which has high affinity for 17 beta-estradiol. We believe that this binding protein represents a P. brasiliensis hormone receptor which can also recognize mammalian estrogens. We hypothesize that the ability of estrogen to decrease or delay mycelium-to-yeast transformation at the initial site of infection contributes to or is responsible for the marked resistance of females, and that the binder described is the molecular site of action. |
Mención de responsabilidad : |
A Restrepo, M E Salazar, L E Cano, E P Stover, D Feldman, D A Stevens |
Referencia : |
Infect Immun. 1984 Nov;46(2):346-53. |
PMID : |
6500694 |
En línea : |
https://iai.asm.org/content/46/2/346.long |
Enlace permanente : |
https://hospitalpablotobon.cloudbiteca.com/pmb/opac_css/index.php?lvl=notice_display&id=4327 |
Estrogens inhibit mycelium-to-yeast transformation in the fungus Paracoccidioides brasiliensis: Implications for resistance of females to Paracoccidioidomycosis [documento electrónico] / Ángela Restrepo Moreno, ; Maria E. Salazar, ; Luz Elena Cano Restrepo, . - 1984. Obra : Infection and ImmunityIdioma : Inglés ( eng) Resumen : |
Evidence that disease due to the thermally dimorphic fungus Paracoccidioides brasiliensis occurs post-puberty predominantly in males led us to hypothesize that hormonal factors critically affect its pathogenesis. We show here that estrogens inhibit mycelial- to yeast-form transformation of P. brasiliensis in vitro. Transformation of three isolates was inhibited to 71, 33, and 19% of the control values in the presence of 10(-10), 10(-8), and 10(-6) M 17 beta-estradiol, respectively. The synthetic estrogen diethylstilbestrol was active but less potent than estradiol, whereas testosterone, 17 alpha-estradiol, tamoxifen, and corticosterone were inactive. This function was specifically inhibited, since yeast-to-mycelium transformation, yeast growth, and yeast reproduction by budding were unaffected by 17 beta-estradiol. Of note is the fact that mycelium-to-yeast transformation occurs as the first step in vivo in the establishment of infection. The cytosol of the three isolates studied possesses a steroid-binding protein which has high affinity for 17 beta-estradiol. We believe that this binding protein represents a P. brasiliensis hormone receptor which can also recognize mammalian estrogens. We hypothesize that the ability of estrogen to decrease or delay mycelium-to-yeast transformation at the initial site of infection contributes to or is responsible for the marked resistance of females, and that the binder described is the molecular site of action. |
Mención de responsabilidad : |
A Restrepo, M E Salazar, L E Cano, E P Stover, D Feldman, D A Stevens |
Referencia : |
Infect Immun. 1984 Nov;46(2):346-53. |
PMID : |
6500694 |
En línea : |
https://iai.asm.org/content/46/2/346.long |
Enlace permanente : |
https://hospitalpablotobon.cloudbiteca.com/pmb/opac_css/index.php?lvl=notice_display&id=4327 |
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