Gene transcription abnormalities in canine atopic dermatitis and related human eosinophilic allergic diseases.

Canine atopic dermatitis (AD) is clinically similar to human AD, implicating it as a useful model of human eosinophilic allergic disease. To identify cutaneous gene transcription changes in relatively early inflammation of canine AD, microarrays were used to monitor transcription in normal skin (n=13) and in acute lesional AD (ALAD) and nearby visibly nonlesional AD (NLAD) skin (n=13) from dogs. Scanning the putative abnormally transcribed genes, several potentially relevant genes, some abnormally transcribed in both NLAD and ALAD (e.g. IL6, NFAM1, MSRA, and SYK), were observed. Comparison for abnormally transcribed genes common to two related human diseases, human AD and asthmatic chronic rhinosinusitis with nasal polyps (aCRSwNP), further identified genes or gene sets likely relevant to eosinophilic allergic inflammation. These included: (1) genes associated with alternatively activated monocyte-derived cells, including members of the monocyte chemotactic protein (MCP) gene cluster, (2) members of the IL1 family gene cluster, (3) eosinophil-associated seven transmembrane receptor EMR1 and EMR3 genes, (4) interferon-inducible genes, and (5) keratin genes associated with hair and nail formation. Overall, numerous abnormally transcribed genes were observed only in canine AD; however, many others are common to related human eosinophilic allergic diseases and represent therapeutic targets testable in dogs with AD.