Deficiency of decorin induces expression of Foxp3 in CD4+CD25+ T cells in a murine model of allergic asthma

Background and objective Decorin (Dcn), an extracellular matrix proteoglycan, has several important biological functions, and its deposition is altered in the airway wall of humans with asthma and animal models of asthma. Due to its high affinity for transforming growth factor beta (TGF)-β, Dcn can function as part of a negative feedback mechanism, resulting in the regulation of this factor's bioavailability. Dcn deficient (Dcn−/−) mice develop reduced airway inflammation, hyperresponsiveness and remodeling in response to repeated allergen challenge; we investigated whether regulatory T cells play a role in the diminished airway response of Dcn−/− mice. Methods Dcn−/− and Dcn+/+ mice (C57Bl/6) were sensitized with ovalbumin (OVA) and challenged intra-nasally 3 days/week × 3 weeks. After allergen challenge, bronchoalveolar lavage was collected to quantify total and differential cell counts and cytokine levels. Inflammatory cell number and cytokine messenger ribonucleic acid (mRNA) production were assessed in lung tissues. Cells from lung and spleen were extracted to evaluate regulatory T cells. Results Tissue inflammation and interleukin (IL)-13 mRNA expression were significantly increased in OVA-challenged Dcn+/+ mice, only. The increased expression of Foxp3 in CD4+CD25+ T cells found in lung of OVA-challenged Dcn−/− mice was accompanied by an increase in IL-10 mRNA. Conclusions Our data demonstrated that a diminished lung inflammation in OVA challenged Dcn−/− mice was accompanied by a higher expression of regulatory T cells and IL-10 mRNA levels. These results reinforce the importance of Dcn in biological processes, particularly in an allergic model of asthma.