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Adhesion activity of L. acidophilus NK1, L. fermentum 90 TS4, and C. albicans 506 B on female vaginal epithelium was studied. Adhesion of various lactobacillus species was hormone-dependent. Adhesion of C. albicans 506 B was not associated with estrogen level. The effects of synthetic drugs and phytopreparations used for hormone replacement on adhesion of vaginal microbiocenosis members varied.

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Phytoestrogens present in the plants endemic for Chile were studied. The effects of phytoextract [specimen of preparation No. 181 (fraction b)] on target tissues were similar to those of estradiol. The preparation inhibited the stimulatory effect of estradiol on vaginal lactobacilli population.

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Since the early reports linking the development of clear cell cervicovaginal adenocarcinoma in young women with diethylstilbestrol treatment of their mothers during pregnancy, it became clear that perinatal exposure to several substances may induce irreversible alterations, that can be detected later in life. Current evidence suggests that these substances induce, by the mechanism of imprinting, alterations of the differentiation of several cell-types, resulting in the development of disease during the adult age. The most known delayed effects to prenatal exposure to agents displaying hormone action, pollutants, food additives and natural food components, substances of abuse and stress by the mechanism of imprinting are described. Among them, estrogens, androgens, progestins, lead, benzopyrenes, ozone, dioxins, DDT, DDE, methoxychlor, chlordecone, parathion, malathion, polychlorobiphenyls, pyrethroids, paraquat, food additives, normal food constituents, tetrahydrocannabinol, cocaine and opiates. It is concluded that perinatal exposure to several agents causes irreversible changes that determine health conditions during adulthood. Several diseases developing during adulthood probably were determined during early stages of life, under the effect of exposure or preferential mother's diet during pregnancy. Regulations to avoid these early exposures may contribute to an important improvement of health conditions of humankind.

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BACKGROUND: The target cellular response to glucocorticoids is proportional to the concentrations or affinity of specific receptors to these substances. AIM: To look for a correlation between glucocorticoid receptor concentrations in synovial wall cells and the clinical response to steroidal treatment in patients with rheumatoid arthritis. PATIENTS AND METHODS: Twenty eight patients with rheumatoid arthritis were studied. Each subject was subjected to a synovial biopsy, in which a dry radioautographic technique for diffusible compounds was used. Patients were treated afterwards with three 500 mg intravenous pulses of methilprednisolone. RESULTS: A mean of 44.8% of synovial cells (range 30.1-62.8%) had binding sites for 3H dexamethasone. All patients had a significant clinical improvement after methylprednisolone. Multiple regression analysis did not show a correlation between clinical response and glucocorticoid receptor concentration. CONCLUSIONS: The lack of association between glucocorticoid receptor concentrations and clinical response could be due to the large steroid dose used, that saturated all available receptors.

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There is increasing body of evidence to suggest that sex hormones may be closely involved in the pathogenesis of autoimmune diseases in humans. In the present article we discuss heteroimmune response differences between males and females and the roles of gender and sex hormones in autoimmune diseases in various species. The general conclusions are the following. Androgens and perhaps progestogens may protect from autoimmune disease; however oestrogens seems to have a dualistic effect on the immune system. Is has been demonstrated that oestrogens suppress antigen-specific T-cell dependent immune reactions while enhance B-cell activities.

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Exposure of animals perinatally to some hormonally active agents may imprint permanent changes on the action of related hormones. The present study investigated the effects of early postnatal androgenization on various genomic responses to estrogen in the uterus of prepubertal rats. Female rats were androgenized at postnatal ages of 1, 5, or 13 days with a single s.c. injection of testosterone propionate. At the age of 21 days, the animals were stimulated with estrogens. The uteri of androgenized and control rats were analyzed morphometrically to measure genomic parameters of estrogen stimulation in the uterus. The results demonstrate that early postnatal androgenization does not equally affect all uterine cell types and that the effects of androgenization change according to the age at androgenization. The dissociation between the various responses according to the time of androgenization suggests that there are critical ages at which the uterine cell types that respond to estrogens can be altered permanently by imprinting. The finding of changes in the action of estrogen induced by androgenization at older than neonatal ages in the rat suggests that similar changes may occur in humans exposed to androgens during their extrauterine life. This result also points to the need for further studies using the rhesus monkey because of its close resemblance to the human with respect to female reproductive physiology.

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Glucocorticoids are known to exert their antiinflammatory effects through an interaction with specific hormone receptors. Progesterone is able to bind to these glucocorticoid receptors exerting either agonistic or antagonistic actions. We have reported that a single intraarticular injection of progesterone exerts a local antiinflammatory action in patients with rheumatoid arthritis (RA), suggesting an agonistic effect of progesterone on local glucocorticoid receptors. To corroborate this possible mechanism of action, we investigated the binding of 3H-dexamethasone to local glucocorticoid receptors in synovial tissue from 3 patients with active RA, before and 14 days after a single intraarticular injection of progesterone. Both cytoplasmic and nuclear 3H-dexamethasone binding sites were observed within synoviocytes, macrophages, fibroblasts, lymphocytes and endothelial cells. Dry radioautograms of biopsied synovial tissue demonstrated a marked decrease of 3H-dexamethasone binding following progesterone treatment in all patients (p less than 0.001 for each comparison). Although the number of cases is not large enough to draw definitive conclusions, our data confirm the marked anti-inflammatory effect of intraarticular progesterone and support the hypothesis of an agonistic effect of progesterone (or its metabolites) on glucocorticoid receptors.

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A role for eosinophils in the immune reaction has not been yet established. Considering that these leukocytes accumulate in lymphoid organs under glucocorticoid stimulation, we explored the possibility that they participate in the depression of immune reactions induced by these hormones and that they degranulate to exert this action. In this context, we investigated the dose effect of three estrogens on the number and degranulation of spleen red pulp eosinophils and on the percentage of spleen cross sectional area comprising white pulp. Estradiol-17 beta or 4 (OH) estradiol-17 beta increased red pulp eosinophils at low doses: 2 (OH) estradiol-17 beta increased them at a very high dose. The three estrogens degranulated the spleen eosinophils and decreased the lymphocyte containing spleen white pulp. We propose that the decrease in white pulp is a response mediated by agents released from degranulating eosinophils under the action of estrogen. Consequently, both estrogen-induced eosinophil degranulation and estrogen-induced increase in red pulp eosinophil numbers are conditions contributing to a decrease in white pulp volume. All above evidence supports the hypothesis that eosinophils are involved in immunoregulation by diminishing the number of lymphocytes contained in lymphoid organs.

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Eosinophil leukocytes migrate from the blood to the uterus under estrogen stimulation, redistribute through uterine extravascular compartment, degranulate in the organ, and release agents that are involved in several parameters of estrogen action. Agents that induce blood eosinopenia, block their migration to the uterus, interfere with their redistribution within the organ or modify their degranulation, selectively interfere with eosinophil-mediated responses to estrogen. The present study investigated whether ketotifen, an antiallergic agent that inhibits allergen-induced eosinophil degranulation, interferes with estrogen-induced eosinophil migration to the uterus and their subsequent degranulation. Ketotifen does not interfere with estrogen-induced eosinophil accumulation in the uterus, but decreases the proportion of eosinophils located in endometrium and inhibits their degranulation. These results suggest that neither histamine, calcium or slow reacting substance of anaphilaxis are involved in eosinophil migration to the uterus. The inhibition by ketotifen of eosinophil degranulation may diminish eosinophil migration through extravascular compartment via a decrease in the release from degranulating eosinophils of enzymes required for this migration. It is possible that the inhibition by ketotifen of both, eosinophil degranulation and eosinophil motility through uterine extravascular compartment, interfere with eosinophil-mediated responses to estrogen or with other functions of these cells.

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Exposure of fetuses to some hormonally active agents may imprint permanent changes on the action of related hormones. These changes can be detected in adulthood as a modification of the degree of responsiveness to hormone action. The present study describes the effect of prenatal androgenization on the various responses to oestrogen in different types of cells in the uterus of prepubertal rats. Prenatal androgenization completely abolishes oestrogen-induced hypertrophy of uterine luminal and glandular epithelium, while it does not interfere with hypertrophy of circular myometrium and potentiates uterine eosinophilia and oedema. This dissociation between the various responses to oestrogen suggests that prenatal androgenization does not equally affect all uterine cell types.

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The antiinflammatory effect of a single intraarticular injection of progesterone was investigated in 12 patients with rheumatoid arthritis. A local, but no systemic decline of inflammation was observed in 10 of them for at least one month. The average local scores of inflammation at Days 7, 14, 21 and 30 after injection were significantly lower than pretreatment scores (p less than 0.000003 for each comparison). In some patients the effect continued for up to 2 months. No important side effects were observed during the following 2 months. However, a more prolonged followup of treated patients is necessary to rule out the late onset of side effects.

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The present study was designed to investigate the dose-response of clomiphene on several estrogenic responses in the immature rat uterus and to compare it to available data on estradiol-17 beta. A dissociation was demonstrated among the different estrogenic responses induced by clomiphene. Very high doses of clomiphene were needed to induce the 6-h uterine eosinophilia and deep endometrial edema, and maximal response levels were not reached at any dose studied. On the contrary, many genomic responses were induced with much lower doses of clomiphene, and maximal response levels were reached with at least the two highest doses of clomiphene. This dissociation is in agreement with the existence of separate groups of responses that are mediated by multiple and independent mechanisms of estrogen action involving different kind of receptors. Luminal epithelial, glandular epithelial, and myometrial hypertrophies were also found to differ with regard to the dose needed to induce this response in each cell type. The dissociation between genomic responses of the different uterine cell types supports the hypothesis of different estrogen receptors for each kind of cell. Clomiphene induces mitoses in the different cell types, but the proportion of mitoses in the cell types was different from that described for estradiol. It is suggested that these differences are also due to differences between receptors involved in cell proliferation.

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The present study describes the effects of oestradiol-17 beta and diethylstilboestrol (DES) on several oestrogenic responses in the immature rat uterus Diethylstilboestrol was weaker than oestradiol in inducing uterine eosinophilia, water imbibition and mitoses, as strong as oestradiol in eliciting epithelial hypertrophy at 24 h after treatment, and stronger than oestradiol in eliciting the reduction of epithelial cell height at 6 h after treatment and myometrial cell hypertrophy at 24 h after treatment. In addition, differences among the mitotic responses to oestrogen of the different uterine cell types were also detected. The above dissociation of the effects of DES and oestradiol-17 beta is in agreement with the hypothesis that eosinophil-mediated non-genomic responses, genomic responses and cell proliferation are mediated by independent mechanisms, involving different receptors which may have different affinities for both compounds. The eosinopenia and eosinophil degranulation under DES treatment suggest an explanation for the effect of DES on water imbibition. The dissociation among genomic responses from the different uterine cell types supports the hypothesis that different kinds of cytosol-nuclear oestrogen receptors exist.

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Oestrogen induces a migration of eosinophil leukocytes to the uterus where, it is suggested, these cells mediate several responses to hormone stimulation. To investigate the mechanism of the recognition of the uterus by the eosinophils, the present study describes the effect of a blockade of the rat reticulo-endothelial system with colloidal carbon on oestrogen-induced uterine eosinophilia, and other responses to oestrogen stimulation that, it has been suggested, are mediated by eosinophils. In the absence of oestrogen colloidal carbon induced an increase in the number of eosinophils in mesometrium but not in endometrium with myometrium, and a slight oedematous reaction in deep endometrium. Colloidal carbon abolished the oestrogen-induced increase in the number of eosinophils in endometrium with myometrium and drastically decreased the oestrogen-induced increase in uterine wet weight and the endometrial oedematous responses 6 h after the administration of oestrogen. The present results agree with the hypothesis that most uterine water imbibition is mediated by eosinophils and suggest a possible mechanism for the interaction of colloidal carbon with eosinophil migration to the uterus.

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This paper describes the induction of uterine eosinophilia as well as of deep endometrial edema and increase of uterine wet weight in the immature rat by the catecholestrogens 2-OH-estradiol and 4-OH-estradiol. These effects are thought to be mediated by eosinophils via a specific eosinophil receptor system. 4-OH-estradiol was equipotent with estradiol, whereas the effect of 2-OH-estradiol was significantly weaker.

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Se ha propuesto que los eosinófilos están involucrados en la mediación de diversas respuestas no gemónicas a sustancias hormonales tales como Estrógenos, Glucocorticoides y Catecolaminas. Considerando que cualquier factor que degranule eosinófilos, afecta las respuestas mediadas por éstos, el objetivo de este trabajo fue estudiar la degranulación de eosinófilos inducida "in vitro" mediante la adición de varias concentraciones de Adrenalina o su vehículo a sangre extraída de la cola de ratas hembras adultas a) ovariectomizadas y b) ovariectomizadas y adrenalectomizadas; degranulación que fue estudiada en varios tiempos de incubación "in vitro". Los resultados muestran que la Adrenalina degranula eosinófilos "in vitro", este efecto es más importante en ratas no adrenalectomizadas que en las adrenalectomizadas, lo que sugiere que la existencia de hormonas de origen suprarrenal induce una mayor cantidad de receptores de adrenalina, de tal manera que los eosinófilos seran más sensibles al efecto degranulatorio de ésta

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