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Gene Transcription Abnormalities in Canine Atopic Dermatitis

ABSTRACT: 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.

ORGANISM(S): Canis lupus familiaris

PROVIDER: GSE39278 | GEO | 2012/07/12

SECONDARY ACCESSION(S): PRJNA170463

REPOSITORIES: GEO

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Gene Transcription Abnormalities in Canine Atopic Dermatitis

Project description: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. Total RNA from skin biopsy specimens from 13 Healthy (i.e. Normal) dogs were compared to total RNA from acute lesional skin biopsy specimens (i.e. ALAD) and nearby visibly nonlesional skin biopsy specimens (i.e. NLAD) from 13 dogs with atopic dermatitis.

2012-07-11 | E-GEOD-39278 | biostudies-arrayexpress

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Project description:The aim of the study was to identify genes which are differentially expressed in the blood of dogs with canine atopic dermatitis (AD) before and after 6 months of allergen-specific immunotherapy (ASIT) in comparison to healthy control dogs. Diagnosis of AD was based on compatible history and clinical signs determined using Willemse and Prélaud diagnostic criteria, completed by Favrot criteria as follows: pruritus sine material, indoor lifestyle and the exclusion of other causes of pruritus ongoing for at least one year. Clinical diagnosis of atopic dermatitis was confirmed by serological allergy testing (IDEXX allergic panel test) and intradermal skin testing (Artuvetrin test set, Netherlands). In order to avoid the role of food antigens as a cause of the skin condition elimination diet was used for 6–8 weeks. No anti-inflammatory drugs were given for at least 3 weeks prior examination with serological test, intradermal test and blood collection. All dogs, which were classified to the investigated group had positive reactions in serological allergy testing and intradermal skin testing. Subsequently, subcutaneous allergen-specific immunotherapy was applied. Allergen extracts were prepared on the basis of the results of intradermal tests by the Artuvetrin company and were administered subcutaneously in increasing concentrations during 6 months according to the manufacturer's recommendations. Aside from gene regulation, this experiment also examined the participation of individual lymphocyte subpopulations (like: B, T, Th, Tc, Treg) and the level of interleukins in the blood of AD dogs before and after therapy.

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