2026-10-12T12:14:21Z https://api.figshare.com/v2/oai

oai:figshare.com:article/34048223 2026-10-01T17:31:13Z category_4 category_7 category_8 category_12 category_14 category_16 category_21 category_873 category_46 category_64 category_132 portal_5 item_type_3 month_year_10_2026

<p>Data.</p> Naim Gheymoumi (25157753) Sevda Shayesteh (25157756) Fatemeh Sharifi (3496619) Marziyeh Amiri-Andebili (25157759) Hediyeh Gheymoumi (25157762) Biochemistry Medicine Microbiology Cell Biology Molecular Biology Physiology Biotechnology Chemical Sciences not elsewhere classified Immunology Cancer Infectious Diseases potential immunometabolic modulator following ova sensitization endogenous tryptophan metabolite elevated serum ige aryl hydrocarbon receptor serum inflammatory markers including increased sneezing mucosal immune regulation systemic inflammatory mediators study investigated kyna findings support kyna marked inflammatory changes xlink "> rats local regulatory cytokines ar remain unclear systemic effects comparable ahr signaling contributes xlink "> regulatory cytokines systemic anti inflammatory infiltration histopathological changes inflammatory effects cytokine regulation associated regulation ahr signaling kyna ), splenic tissues splenic histopathology kynurenic acid indicating involvement immunomodulatory properties greater improvement epithelial damage behavioral responses associated proteins <div> <p>Background</p><p>Allergic rhinitis (AR) is a chronic inflammatory airway disease characterized by dysregulated type 2 immune responses and impaired mucosal immune regulation. Kynurenic acid (KYNA), an endogenous tryptophan metabolite with immunomodulatory properties, may influence inflammatory pathways, but its mechanisms in AR remain unclear. This study investigated KYNA in an ovalbumin (OVA)-induced rat model of AR and examined the role of aryl hydrocarbon receptor (AhR) signaling.</p> <p>Methods</p><p>Rats were assigned to control, AR, vehicle, KYNA, desloratadine, and KYNA + AhR antagonist (CH223191) groups. Following OVA sensitization and challenge, behavioral responses, serum inflammatory markers, nasal AhR-associated proteins, regulatory cytokines, and histopathological changes in nasal and splenic tissues were evaluated.</p> <p>Results</p><p>OVA induced typical allergic responses, including increased sneezing and nasal scratching, elevated serum IgE, IL-4, and IL-6, and marked inflammatory changes in nasal and splenic tissues. KYNA significantly reduced behavioral symptoms, systemic inflammatory mediators, epithelial damage, and inflammatory infiltration, with systemic effects comparable to desloratadine but greater improvement in nasal scratching and splenic histopathology. KYNA restored nasal AhR and CYP1A1 expression and increased IL-10 and TGF-β, whereas CH223191 partially attenuated these effects, indicating involvement of AhR signaling. Desloratadine showed limited effects on local regulatory cytokines. Histopathological analysis confirmed improved nasal and splenic architecture following KYNA treatment.</p> <p>Conclusion</p><p>In conclusion, KYNA attenuates experimental AR through systemic anti-inflammatory effects and restoration of mucosal immune regulation. AhR signaling contributes to these effects, particularly in CYP1A1 and cytokine regulation, while additional mechanisms may also be involved. These findings support KYNA as a potential immunometabolic modulator in allergic airway disease.</p></div> 2026-10-01T17:31:10Z Dataset Dataset 10.1371/journal.pone.0359624.s001 https://figshare.com/articles/dataset/_p_Data_p_/34048223 CC BY 4.0