No abstract

Keratinocyte-derived cytokines such as thymus and activation-regulated chemokine, granulocyte-macrophage colony stimulating factor, thymic stromal lymphopoietin and interleukin-33 are involved in the pathogenesis of human AD and possibly in canine AD. These cytokines and chemokines may possibly be used as subjective clinical markers and therapeutic targets for both human and canine AD.

Background-Thymus and activation-regulated chemokine (TARC/CCL17) has been implicated in the pathogenesis of canine atopic dermatitis (cAD). Serum TARC concentrations are a reliable biomarker for human atopic dermatitis; however, their potential as a biomarker for cAD has not been investigated. Hypothesis/Objectives-To investigate whether serum TARC concentrations correlate with disease severity and therapeutic responses for cAD. Animals-Thirty-nine dogs with cAD and 42 healthy dogs were recruited. Methods and materials-Serum TARC concentrations in dogs with cAD and healthy dogs were measured by sandwich ELISA with anti-canine TARC antibodies. The clinical severity of cAD was scored using the validated Canine Atopic Dermatitis Extent and Severity Index, 4th iteration (CADESI-04). Serum TARC concentrations were compared between dogs with cAD and healthy controls, and their relationship with CADESI-04 was examined. Serum TARC concentrations also were measured in 20 dogs with cAD treated with prednisolone or oclacitinib for four weeks. Results-Serum TARC concentrations were significantly higher in dogs with cAD than in healthy dogs (P < 0.001). In dogs with cAD, serum TARC concentrations correlated with CADESI-04 scores (q = 0.457, P < 0.01). Furthermore, serum TARC concentrations significantly decreased in treated dogs with the attenuation of clinical signs (P < 0.001). Changes in serum TARC concentrations before and after treatment correlated with those in CADESI-04 scores (q = 0.746, P < 0.001). Conclusions and clinical relevance-Serum TARC concentrations have potential as a clinical and research tool for the objective evaluation of disease severity and therapeutic responses for cAD.

The results indicate that IL-33 is involved in chronic lesional skin of cAD.

Keratinocytes activated by IL-17A have the ability to produce various pro-inflammatory cytokines and chemokines, suggesting that IL-17A may play a central role of the development of Th2-associated inflammation in canine AD.