Indolepropionic acid modulates the immune response in allergic rhinitis through the AKT/CEBPB/IL‑10 signaling pathway

Allergic rhinitis (AR) is a common inflammatory disorder of the nasal mucosa, usually triggered by environmental allergens. Indolepropionic acid (IPA) can influence immune responses; however, the specific mechanisms underlying the effects of IPA on immune regulation in AR remain largely unexplored. In the present study, an experimental mouse model of AR was established by sensitizing and exposing the mice to allergens, followed by the administration of IPA via gavage. Nasal symptoms were assessed through behavioral scoring, histological examinations were conducted to evaluate changes in nasal mucosa, and cytokine levels were quantified using ELISA. The expression of key signaling molecules was analyzed by immunohistochemistry, reverse transcription‑quantitative PCR and western blotting. Additionally, the effects of IPA combined with an Akt Inhibitor (HY‑10355) on signaling pathway‑related proteins in human nasal epithelial cells were evaluated using cellular immunofluorescence and western blotting. The results revealed that IPA treatment significantly reduced nasal inflammation, as indicated by decreased sneezing and mucus secretion. Histological analysis showed reduced inflammatory cell infiltration and epithelial damage in IPA‑treated mice compared to controls. Furthermore, cytokine analysis revealed reduced levels of the pro‑inflammatory cytokines IL‑4, IL‑5, IL‑13 and immunoglobulin E, along with increased levels of the anti‑inflammatory cytokine IL‑10. Molecular investigations demonstrated that IPA can activate the Akt/CCAAT enhancer binding protein β pathway, leading to increased IL‑10 expression and reduced inflammation. In conclusion, these findings suggested that IPA may serve as a promising therapeutic strategy for managing AR, pending further clinical validation.

AKT/CCAAT enhancer binding protein β/IL‑10 pathway; allergic rhinitis; immune modulation; indolepropionic acid; inflammatory response.