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B, Total BALF cell numbers were increased after 3 and 6 weeks of HDM exposure compared to saline controls and were even higher after Rapa treatment compared to HDM

Posted on October 28, 2021 By scienzaunder18

B, Total BALF cell numbers were increased after 3 and 6 weeks of HDM exposure compared to saline controls and were even higher after Rapa treatment compared to HDM. Rapamycin treatment prevented this increase in IgE after HDM re-exposure, but dexamethasone treatment did not. HDM-specific IgG1 was increased in HDM exposed mice after 6 weeks of rest/recovery (group 2). There was no further increase in IgG1 after HDM re-exposure. Accordingly, neither rapamycin nor dexamethasone treatment suppressed HDM-specific IgG1 levels in the serum (group 3). Open in a separate window Figure 2 Protocol 1- Allergic sensitization, inflammatory cell numbers in the BALF, and AHR NVP-BHG712 after HDM re-exposure. Total numbers of macrophages and eosinophils were increased after HDM re-exposure (group 3), but not in HDM rest NVP-BHG712 (group 2) animals in the BALF. Total neutrophil numbers in the BALF were slightly increased after HDM re-exposure in Rapa treated mice. Rapa did not suppress HDM-induced increases in eosinophils. Eosinophil numbers were lower in Dex treated mice compared to HDM re-exposed and Rapa treated groups, but still higher then saline control (Lung effector T cells (CD44+Foxp3?) were increased after HDM re-exposure and attenuated by Rapa and Dex (CD44+Foxp3? effector cells, as a percentage of total CD4+ T cells were increased in all HDM re-exposed groups and not suppressed by Rapa or Dex (Levels of INF- appeared to be lower after rapamycin (Rapa) treatment in HDM re-exposed mice, but were not statistically different between any of the groups (P-S6, a downstream mediator of mTOR complex 1 signaling, was increased in HDM re-exposed mice (group 3) and this was blocked by rapamycin (Rapa) treatment (Total CD4+ T cells were increased after 6 weeks of HDM and suppressed by rapamycin (Rapa) and dexamethasone (Dex) (CD69+Foxp3? activated T cells, when assessed as a percentage of total CD4+ T cells, were increased after HDM exposure and unaffected by Rapa and Dex (CD44+Foxp3? effector T cells, when expressed as a percentage of total CD4+ T cells, were increased after HDM exposure and attenuated by Rapa and Dex (Total lung regulatory T cells (Foxp3+CD25+) were increased after chronic HDM exposure and suppressed by Rapa and Dex (The ratio of regulatory T cells Foxp3+CD25+ to CD44+Foxp3? effector T cells was decreased in HDM exposed mice compared to saline controls (they still suggest that rapamycin could have direct effects on B cells, which could account for the decreases in IgE levels in our model and therefore reduce sensitization to HDM, despite increased IL-4. When we assessed B cells in the lung tissue, there was a trend towards a decrease in B cells in both studies after rapamycin treatment. Despite being non-significant, we cannot exclude that this minor decrease in lung B cell levels could contribute to the observed decrease in IgE levels. The source of the IL-4 increase is unclear in our model since T cells, which are one of the primary sources of IL-4, were reduced. Other cells including eosinophils, basophils, and mast cells can secrete IL-4 [35], but whether these cells are playing a role in enhancing IL-4 levels in our model is unclear. Also in our study, eotaxin 1, an NVP-BHG712 important epithelial cell derived eosinophil chemokine, remained elevated in the BALF with rapamycin treatment, which may explain why eosinophil numbers were not suppressed. This NVP-BHG712 was also true in our previous acute study in which Mouse monoclonal to CEA rapamycin treatment did not suppress airway inflammation nor eotaxin 1 levels once sensitization was established [18]. More recent studies have indicated an important role for regulatory T cells in the resolution of allergic airway disease [36], [37], [38]..

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