Effect of Retinoic Acid in a Mouse Model of Allergic Rhinitis

• Published in: Allergy, asthma & immunology research 2015, Asthma & Immunology Research, 7(6), , pp.590-598
• Main Authors: Son, Hye Lim, Park, Hyang Rim, Park, Yong Jin, Kim, Soo Whan
• Format: Article
• Language: English
• Subjects: Dermatophagoides; Original; 내과학
• ISSN: 2092-7355; 2092-7363
• DOI: 10.4168/aair.2015.7.6.590

All-trans retinoic acid (ATRA) modulates immune responses by affecting T cells. Several studies have revealed that allergic inflammation of the lower airways is negatively associated with the vitamin A concentration. However, the role of ATRA in allergic inflammation of the upper airways is unclear. We investigated the effects of ATRA in an allergic rhinitis mouse model. BALB/c mice except control groups (CON group) were sensitized with and challenged intra-nasally with Dermatophagoides farina (AR group). The ATRA groups were administered ATRA intraperitoneally. The steroid groups were administered steroid intranasally (ST group). Allergic symptoms and the average eosinophil number were counted. Cytokines and transcription factors were measured by Real-Time PCR and Western blotting. Der f-specific immunoglobulin E (IgE) was measured. Flow cytometry results of CD4⁺CD25⁺Foxp3⁺ T cells were analyzed. The symptom scores were lower in the ATRA group than in the AR group and higher than in the CON group. The levels of IgE were lower in the ATRA group than in the AR group and higher than in the CON and ST groups. The levels of Foxp3, TGF-β, and IL-10 mRNA, as well as the percentage of CD4⁺CD25⁺Foxp3⁺ T cells, were higher in the ATRA group than in theAR group. In the ATRA group the levels of IFN-γ mRNA were higher, and the levels of GATA-3 and IL-4 mRNA, and ROR-γt were lower. In Western blotting analyses, the expression patterns of all factors, except Foxp3, showed similar to those of mRNA expression. ATRA has anti-allergic effects in an allergic rhinitis model, and its underlying mechanisms mainly include the induction of regulatory T cells and the inhibition of Th2 responses.