BACKGROUND: Canine atopic dermatitis (cAD) is a common condition in dogs that may be a naturally occurring model for human atopic dermatitis (hAD). Despite this, comparative research is limited, particularly into the genetic background of cAD. OBJECTIVES: 1. Measure candidate gene expression in cAD skin using quantitative real time PCR (qPCR). 2. Correlate gene expression to clinical cAD scores (Canine Atopic Dermatitis Extent and Severity Index[CADESI]-03 and intradermal allergen test [IDT]). METHODS: mRNA was extracted from biopsies of non-lesional and lesional skin from atopic dogs, and healthy skin from non-atopic dogs. Gene expression was quantified using qPCR, and compared between non-lesional atopic, lesional atopic and healthy skin. Gene expression in atopic skin was correlated with clinical severity (CADESI-03) and the number of positive reactions on an IDT. RESULTS: Of the 20 quantified genes, 11 demonstrated statistically significant altered mRNA expression between atopic and healthy skin; dipeptidyl-peptidase-4 (DPP4), phosphatidylinositol-3,4,5-trisphosphate-5-phosphatase-2 (INPPL1), serine protease inhibitor kazal type-5 (SPINK5), sphingosine-1-phosphate lyase-1 (SGPL1), peroxisome proliferator-activated receptor gamma (PPARgamma), S100 calcium-binding protein A8 (S100A8), Plakophilin-2 (PKP2), Periostin (POSTN), Cullin4A, TNF-alpha and metalloproteinase inhibitor-1 (TIMP-1). Three genes correlated with CADESI-03: serum amyloid A 1 (SAA-1), S100A8, and PKP2; and four with IDT results: mast cell protease I (CMA1), SAA-1, S100A8 and SPINK5. CONCLUSION: Genes with altered expression included those relevant to skin barrier formation and immune function, suggesting both are relevant in the pathogenesis of AD. Many of these genes reflect the proposed pathogenesis in hAD, supporting the use of dogs as a model for hAD. Furthermore, these genes may be considered suitable targets for future genetic and protein function studies in human and canine AD.
BACKGROUND:Canineatopic dermatitis (cAD) is a common condition in dogs that may be a naturally occurring model for humanatopic dermatitis (hAD). Despite this, comparative research is limited, particularly into the genetic background of cAD. OBJECTIVES: 1. Measure candidate gene expression in cAD skin using quantitative real time PCR (qPCR). 2. Correlate gene expression to clinical cAD scores (CanineAtopic Dermatitis Extent and Severity Index[CADESI]-03 and intradermal allergen test [IDT]). METHODS: mRNA was extracted from biopsies of non-lesional and lesional skin from atopic dogs, and healthy skin from non-atopic dogs. Gene expression was quantified using qPCR, and compared between non-lesional atopic, lesional atopic and healthy skin. Gene expression in atopic skin was correlated with clinical severity (CADESI-03) and the number of positive reactions on an IDT. RESULTS: Of the 20 quantified genes, 11 demonstrated statistically significant altered mRNA expression between atopic and healthy skin; dipeptidyl-peptidase-4 (DPP4), phosphatidylinositol-3,4,5-trisphosphate-5-phosphatase-2 (INPPL1), serine protease inhibitor kazal type-5 (SPINK5), sphingosine-1-phosphate lyase-1 (SGPL1), peroxisome proliferator-activated receptor gamma (PPARgamma), S100 calcium-binding protein A8 (S100A8), Plakophilin-2 (PKP2), Periostin (POSTN), Cullin4A, TNF-alpha and metalloproteinase inhibitor-1 (TIMP-1). Three genes correlated with CADESI-03: serum amyloid A 1 (SAA-1), S100A8, and PKP2; and four with IDT results: mast cell protease I (CMA1), SAA-1, S100A8 and SPINK5. CONCLUSION: Genes with altered expression included those relevant to skin barrier formation and immune function, suggesting both are relevant in the pathogenesis of AD. Many of these genes reflect the proposed pathogenesis in hAD, supporting the use of dogs as a model for hAD. Furthermore, these genes may be considered suitable targets for future genetic and protein function studies in human and canineAD.
Authors: Joana B Roque; Caroline A O'Leary; David L Duffy; Myat Kyaw-Tanner; Puya Gharahkhani; Linda Vogelnest; Kenneth Mason; Michael Shipstone; Melanie Latter Journal: Immunogenetics Date: 2011-10-12 Impact factor: 2.846
Authors: Lukasz Japtok; Katrin Schaper; Wolfgang Bäumer; Heinfried H Radeke; Se Kyoo Jeong; Burkhard Kleuser Journal: PLoS One Date: 2012-11-08 Impact factor: 3.240