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

Background and objectiveDecorin (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)-, 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. MethodsDcn(-/-) and Dcn(+/+) mice (C57Bl/6) were sensitized with ovalbumin (OVA) and challenged intra-nasally 3 days/weekx3 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. ResultsTissue 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. ConclusionsOur 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. Decorin-deficient (Dcn(-/-)) mice develop a reduced airway inflammation, hyperresponsiveness and remodelling. We evaluated the role of regulatory T cells in Dcn(-/-) mice. The diminished inflammation in Dcn(-/-) OVA-challenged mice was associated with an increase in airway epithelial cell phospho-Smad2 staining, Foxp3 expression in T cells and IL-10 messenger ribonucleic acid (mRNA) expression.