IFATS Collection: Immunomodulatory Effects of Adipose Tissue-Derived Stem Cells in an Allergic Rhinitis Mouse Model

Author:

Cho Kyu-Sup1,Park Hye-Kyung2,Park Hee-Young1,Jung Jin Sup3,Jeon Seong-Gyu4,Kim Yoon-Keun4,Roh Hwan Jung1

Affiliation:

1. Department of Otorhinolaryngology, Medical Research Institute, Pusan National University School of Medicine, Busan, Korea

2. Department of Internal Medicine, Institute of Allergy and Clinical Immunology, Medical Research Institute, Pusan National University School of Medicine, Busan, Korea

3. Department of Physiology, Medical Research Institute, Pusan National University School of Medicine, Busan, Korea

4. Department of Life Science, Postech Biotech Center, Pohang University of Science and Technology, Pohang, Korea

Abstract

Abstract Adipose tissue-derived stem cells (ASCs) exhibit immunosuppressive effects in allogeneic transplantation. However, there is no report that evaluates the in vivo immune-modulating effect of ASCs in an experimental allergic rhinitis (AR) model. We investigated whether ASCs migrate to the nasal mucosa in an AR mouse model and evaluated the immune-modulating effect of ASCs in the AR mouse model. Cultured ASCs (2 × 106) were injected i.v. before the first allergen challenge in the AR mouse model. Migration of ASCs to the nasal mucosa was evaluated by immunofluorescence. The immunomodulatory effects of ASCs were evaluated by nasal symptoms, histology, serum ovalbumin (OVA)-specific antibody, and the cytokine profile of the spleen. ASCs migrated to the nasal mucosa in the AR mouse model. ASCs significantly reduced allergic symptoms and inhibited eosinophilic inflammation in the nasal mucosa. ASCs significantly decreased the serum allergen-specific IgE level and the IgG1/IgG2a ratio and significantly increased the IgG2a level in the AR mouse model. ASCs inhibited interleukin (IL)-4 and IL-5 production from OVA-incubated splenocytes, but enhanced interferon-γ production. In conclusion, ASCs can migrate to the nasal mucosa in the AR mouse model and inhibit eosinophilic inflammation partly via shifting to a T-helper 1 (Th1) from a Th2 immune response to allergens.

Publisher

Oxford University Press (OUP)

Subject

Cell Biology,Developmental Biology,Molecular Medicine

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