We evaluated the role of estradiol and progesterone on the allergic lung inflammation. Rats were ovariectomized (OVx) and seven days later were sensitized with ovalbumin (OA) and challenged two weeks later by OA inhalation; studies were performed 1 day thereafter. OVx-allergic rats developed a reduced pulmonary cellular recruitment in bronchoalveolar lavage (BAL) relative to sham-OVx allergic rats, similarly to observed in intact allergic rats treated with ICI-182,780. Estradiol treatment increased the recovered cells in BAL of OVx-allergic rats, whereas progesterone determined additional reduction. Cells of BAL and bone marrow (BM) of OVx-allergic rats released elevated amounts of IL-10 and reduced IL-1 and TNF-. BM cells of OVx-allergic rats released increased IL-10 and lower IL-4 levels. In BM cells, estradiol treatment of OVx-allergic rats decreased the release of IL-10 but increased that of IL-4. Besides, it caused also an increased release of IL-1 and TNF- by BAL cells. Progesterone significantly increased the release of IL-10, IL-1 and TNF- by BAL cells and augmented that of IL-4 by BM cells. Begranulation of bronchial mast cell OVx rats was reduced after in vitro challenge, an effect reverted by estradiol but not by progesterone. We suggest that serum estradiol:progesterone ratio might drive cellular recruitment, modulating the pulmonary allergy and the profile of anti-inflammatory or inflammatory cytokines release. The existence of such dual hormonal effects might suggest that the hormone therapy of asthmatic post-menopausal women and those suffering of premenstrual asthma should take into account the possibility of worsening the pulmonary conditions.