letto Willow, grazie! Dunque, da quello che ho ricercato, la candida possiede due tipi di recettori, uno per gli estrogeni e un altro per il progesterone; per quest'ultimo però c'è un po' di confusione. In realtà la candida ama nutrirsi di glicogeno. Ho inserito tutto quello che ho ricercato oggi nel link sulla candida, spero sia utile. Inoltre riporto questo:
Candida albicans, an opportunistic dimorphic fungal pathogen
of major medical importance, has both an estrogenbinding
protein (EBP) that displays high affinity for estradiol
and estrone (1) and a corticosteroid-binding protein that
exhibits high affinity for corticosterone and progesterone (2,
3). Our laboratory has also identified EBPs in Saccharomyces
cerevisiae (4, 5) and Paracoccidioides brasiliensis (6, 7)
and a progesterone-binding protein in Trichophyton mentagrophytes
(8-10). We have recently reported the cloning of
the gene encoding the C. albicans corticosteroid-binding
protein and have found a dinucleotide-binding motif within
this protein, suggesting that the corticosteroid-binding protein
may be a flavoprotein with enzymatic activity (11).
When a fungal organism that harbors one of these steroidbinding
proteins is exposed to the cognate hormone, direct
physiological responses have been elicited. Estrogens have
been shown to inhibit the growth of S. cerevisiae (12) and to
block the dimorphic conversion of the mycelial form to the
invasive yeast form in P. brasiliensis (6, 7). Furthermore,
progesterone has been shown to inhibit the growth of T.
mentagrophytes (8-10). In C. albicans, estradiol directly
timulates the dimorphic transition from the yeast to the
hyphal form (13) and because the latter form is associated
with tissue invasion, this hormonal action may increase
fungal virulence. In contrast, other steroid hormones that
bind poorly to the steroid-binding proteins do not elicit these
biological responses. These in vitro hormone actions, mediated
by mammalian steroids when directly applied to the
microorganisms, have led us to speculate that the hormonal
environment ofthe host may similarly affect the growth of an
invading pathogen and thereby possibly modify its infectivity
or pathogenicity (14). In humans, it is generally accepted that
exposure to elevated levels of estrogens or corticosteroids
leads to an increase in susceptibility to fungal infection. This
effect is usually attributed to the hormonal action to impair
host defenses (15, 16). In addition to effects on the host, our
hypothesis raises the possibility of direct actions of circulating
hormones on the fungal pathogen, mediated by an interaction
with the steroid-binding proteins present in various
organisms. To investigate this hypothesis we have purified an
EBP from C. albicans and cloned the gene that encodes this
protein.
Proc. Nati. Acad. Sci. USA
Vol. 91, pp. 922-926, February 1994
Microbiology
Candida albicans estrogen-binding protein gene encodes an
oxidoreductase that is inhibited by estradiol
(steroid hormones/flavoprotelns/old yellow enzyme/cxpresslo/cloning
NAHID D. MADANI, PETER J. MALLOY, PILAR RODRIGUEZ-POMBO, ARUNA V. KRISHNAN,
AND DAVID FELDMAN*
Division of Endocrinology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305
Communicated by David D. Perkins, October 11, 1993 (received for review August 4, 1993)
