Previous studies from our lab demonstrated that HDM-induced allergic asthma could be prevented if rapamycin was administered early and simultaneously with HDM. In this case, rapamycin prevented HDM-induced AHR, inflammation, goblet cells, and allergic sensitization. Since allergic sensitization was suppressed in our previous studies, we also determined whether rapamycin could prevent allergic responses once sensitization had already been established. To do this, mice were first sensitized systemically to HDM by i.p. injection. Mepiroxol during subsequent intranasal HDM exposures, mice were treated with rapamycin. In this case, rapamycin still suppressed many of the key allergic responses including IgE, AHR, goblet cells, T cell responses, and key mediators like IL-13 and leukotrienes, although it did not suppress increases in inflammatory cells in the BALF, which may have partly been due to the chemokine, eotaxin 1, since levels were still elevated after rapamycin treatment. Although these studies demonstrated an important role for the mTOR pathway during early allergic sensitization and asthmatic disease processes, it was unclear whether mTOR signaling would be important during allergen re-exposure or during established/Albaspidin-AA progressive allergic disease. The studies we report in this manuscript sought to address this question. These data suggests that the role of mTOR is very different depending on the timing/disease stage since rapamycin treatment during allergen re-exposure or during chronic, ongoing disease did not attenuate key characteristics of allergic asthma including AHR and inflammation and actually augmented IL-4 and eotaxin 1 levels. The results from our second protocol are similar to that of a recent study published by Fredriksson et. al. who demonstrated that rapamycin did not suppress allergic responses when administered during chronic allergic disease. In addition, our studies demonstrated that rapamycin suppressed T cells in the lung tissue, including regulatory T cells and our studies also compared the effects of rapamycin to the steroid, dexamethasone. Allergic asthma is often treated with steroids to suppress inflammation. Previous studies have utilized the corticosteroid, dexamethasone, in allergic asthma models. For example, a study similar to ours investigated the effects of dexamethasone during allergic relapse and overt disease. In an OVA model of allergic airway disease, dexamethasone suppressed goblet cells, serum IgE, AHR, and reduced airway inflammation in a relapse model. During overt disease, dexamethasone reduced goblet cells, AHR, and the number of eosinophils, but had no effect on serum IgE levels. In our HDM-induced model of allergen re-exposure/relapse, dexamethasone also decreased goblet cells, but did not suppress IgE or AHR and eosinophil numbers were only slightly reduced. Likewise, during chronic, ongoing or overt disease, we did not observe suppression of goblet cells and the effects on AHR were limited, although there were decreases in inflammatory cell numbers, specifically eosinophils. Although the decrease in eosinophils in this study was as expected with dexamethasone treatment, no decrease in AHR was surprising. However, previous reports have suggested that the timing of AHR measurements after dexamethasone treatment may be important. Specifically, when AHR was measured 12 hours after dexamethasone treatment, AHR was suppressed, but by 24 hours after dexamethasone treatment, AHR was no longer suppressed.