Abstract
BackgroundFluctuations of estradiol and progesterone levels caused by the menstrual cycle worsen asthma symptoms. Conflicting data are reported in literature regarding pro and anti-inflammatory properties of estradiol and progesterone.MethodsFemale Wistar rats were ovalbumin (OVA) sensitized 1 day after resection of the ovaries (OVx). Control group consisted of sensitized-rats with intact ovaries (Sham-OVx). Allergic challenge was performed by aerosol (OVA 1%, 15 min) two weeks later. Twenty four hours after challenge, BAL, bone marrow and total blood cells were counted. Lung tissues were used as explants, for expontaneous cytokine secretion in vitro or for immunostaining of E-selectin.ResultsWe observed an exacerbated cell recruitment into the lungs of OVx rats, reduced blood leukocytes counting and increased the number of bone marrow cells. Estradiol-treated OVx allergic rats reduced, and those treated with progesterone increased, respectively, the number of cells in the BAL and bone marrow. Lungs of OVx allergic rats significantly increased the E-selectin expression, an effect prevented by estradiol but not by progesterone treatment. Systemically, estradiol treatment increased the number of peripheral blood leukocytes in OVx allergic rats when compared to non treated-OVx allergic rats. Cultured-BAL cells of OVx allergic rats released elevated amounts of LTB4 and nitrites while bone marrow cells increased the release of TNF-α and nitrites. Estradiol treatment of OVx allergic rats was associated with a decreased release of TNF-α, IL-10, LTB4 and nitrites by bone marrow cells incubates. In contrast, estradiol caused an increase in IL-10 and NO release by cultured-BAL cells. Progesterone significantly increased TNF- α by cultured BAL cells and bone marrow cells.ConclusionsData presented here suggest that upon hormonal oscillations the immune sensitization might trigger an allergic lung inflammation whose phenotype is under control of estradiol. Our data could contribute to the understanding of the protective role of estradiol in some cases of asthma symptoms in fertile ans post-menopausal women clinically observed.
Highlights
Compelling evidence indicates that female sex hormones play a role in healthy airway function and during inflammation
Using a rat model of allergic lung inflammation, we have demonstrated that antigen sensitization 7 days after ovaries removal culminates in a drastically decreased cell recruitment into lungs after antigen challenge [25]
To examine that we investigated the magnitude of allergic lung inflammation and the release of inflammatory mediators in female rats sensitized to antigen 1 day after ovariectomy
Summary
Compelling evidence indicates that female sex hormones play a role in healthy airway function and during inflammation. In the context of airway dysfunction, it is noteworthy that oscillations of sex hormones caused by the menstrual cycle might be linked to asthma deterioration [1,2]. Forced expiratory volume and vital capacity are higher during early luteal phase, when estradiol and progesterone levels are high [8]. Overall, these data reinforce the inverse correlation between female sex hormone levels and deterioration of asthma symptoms. Of interest is the data reporting that menstrual cycle, contraceptive usage and hormonal replacement therapy account for asthma deterioration in women [9,10,11,12,13,14], a fact whose mechanisms are yet unclear. Conflicting data are reported in literature regarding pro and anti-inflammatory properties of estradiol and progesterone
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