Conjunctival allergic inflammation involving the interleukin-23/T helper type 17 immune axis in an experimental allergic conjunctivitis mouse model.

To investigate the role of the interleukin-23 (IL-23)/T helper type 17 (Th17) immune axis in conjunctival allergic inflammation using a murine model of experimental allergic conjunctivitis (EAC). Experimental study. BALB/c mice were assigned to four groups: control (untreated), allergy (EAC), IL-23 (EAC with IL-23 eyelid injection), and non-sensitized IL-23 (non-sensitized with IL-23 eyelid injection). Conjunctival tissue was analyzed histologically to quantify eosinophil and neutrophil infiltration. Gene expression of mRNA in conjunctival tissue was assessed using a PCR array and quantitative RT-PCR. Eosinophilic and neutrophilic infiltration in the subconjunctival tissue was more pronounced in the IL-23 group than in the allergy and control groups. PCR array and quantitative RT-PCR analyses revealed significantly elevated Ccl17/Tarc mRNA expression in the IL-23 group compared to the allergy group. IL-17A mRNA, undetectable in the allergy group, was expressed in the IL-23 group. Additionally, PCR array comparisons between the IL-23 and non-sensitized IL-23 groups showed a significant increase in Rorc and Il1r1 expression in the IL-23 group. At the same time, Mmp3, Ccl7, and Ccr2 were significantly upregulated in the non-sensitized IL-23 group. RT-PCR analysis also demonstrated higher IL-17A mRNA levels in the non-sensitized IL-23 group than in the IL-23 group. IL-23 induces mixed eosinophilic-neutrophilic inflammation in conjunctival tissue, characterized by enhanced Th2 and weak Th17 responses in a murine model of EAC. These findings suggest a modulatory role of the IL-23/Th17 axis in influencing the severity and phenotype of allergic conjunctival inflammation.