Materials and Methods: C57BL/6 mice were sensitized to OVA by intraperitoneal injection and challenged intranasally with OVA. To evaluate the effect of ASCs-derived secretome on allergic airway disease, 1 μl/ml of ASCs supernatant were administrated intranasally before OVA challenge. We evaluated airway hyperresponsiveness (AHR), the proportion of eosinophils in bronchoalveolar lavage fluid (BALF), lung histology, serum total and OVA-specific antibody, cytokine profile of BALF and lung draining lymph nodes (LLN), and T cell population of LLN.
Results: ASCs-derived secretome significantly inhibited eosinophilic inflammation in the lung. AHR, total immune cell and eosinophils in the BALF, and mucus production were significantly reduced after ASCs-derived secretome administration. ASCs-derived secretome significantly decreased the serum total and allergen-specific IgE and IgG1 level. ASCs-derived secretome significantly inhibited Th2 cytokines (IL-4, IL-5, and IL-13) and enhanced Th1 cytokine (IFN-γ) and regulatory cytokines (IL-10 and TGF-β) in the BALF and LLN. In addition, CD25+Foxp3+ and IL-10+ T cells in LLN were significantly increased after ASCs-derived secretome administration.
Conclusions: ASCs-derived secretome ameliorated allergic airway inflammation and improved lung function through the induction of Tregs expansion. Secretome may be a promising candidate for a novel cell-free therapy for allergic airway diseases that has many advantages in overcoming the limitations and risks associated with the cell-based therapeutics.