Abstract
Canine atopic dermatitis is a common chronic inflammatory skin disease characterized by pruritus and recurrent erythema, yet objective blood biomarkers for monitoring disease activity remain limited. In this study, we evaluated serum cytokine profiles and their associations with clinical severity in client-owned dogs with atopic dermatitis. A total of 143 dogs were enrolled, including 28 healthy and 115 dogs with atopic dermatitis. The atopic dermatitis group was further categorized into untreated dogs (n = 27; no systemic therapy for ≥4 weeks) and systemically treated dogs (n = 88). Serum concentrations of IFN-γ, IL-10, IL-13, IL-31, and TGF-β1 were measured using an enzyme-linked immunosorbent assay. Group differences were assessed using the Kruskal–Wallis test with Bonferroni-adjusted post hoc comparisons, and correlations with the pruritus visual analog scale (pVAS) and the Canine Atopic Dermatitis Extent and Severity Index-04 (CADESI-04) were analyzed using Spearman’s rank correlation. Serum IFN-γ, IL-13, and IL-31 concentrations differed significantly among groups (p < 0.001, p = 0.001, and p = 0.004, respectively). IFN-γ and IL-13 concentrations were lower in treated dogs than in healthy dogs and untreated dogs, whereas IL-31 concentrations were higher in dogs with atopic dermatitis than in healthy dogs, regardless of treatment status. In correlation analyses, the pVAS showed a negative correlation with IFN-γ (r = −0.239, p = 0.004) and a positive correlation with IL-31 (r = 0.173, p = 0.039), while CADESI-04 showed a negative correlation with IFN-γ (r = −0.252, p = 0.002). IL-10 and TGF-β1 did not show significant differences among groups or correlations with clinical indices. These findings suggest that serum IL-31 may reflect pruritus-related immune signaling that can persist despite clinical improvement. While IFN-γ may show a weak negative correlation with clinical severity indices, its potential association with chronic dermatologic changes, such as lichenification, requires further investigation in relation to disease chronicity. Together, these results indicate that circulating cytokine profiles and clinical indices do not necessarily change in parallel and that selected cytokines may provide complementary information when interpreting disease activity in canine atopic dermatitis. These profiles should be interpreted while considering the diverse immunomodulatory mechanisms of the systemic therapy administered.