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The skin microbiome in allergen-induced canine atopic dermatitis.
Veterinary Dermatology 2016 October
BACKGROUND: Studies focusing on next-generation sequencing of the bacterial 16S rRNA gene have allowed detailed surveys of skin bacterial populations (microbiota) of the skin.
HYPOTHESIS/OBJECTIVES: This study evaluated temporal changes in the skin microbiota in a canine model of atopic dermatitis.
ANIMALS: Eight atopic dogs previously sensitized with house dust mites (HDM).
METHODS: The dogs were topically challenged on the right groin with HDM allergens. Swabs were collected from the challenged and the contralateral nonchallenged sites prior to provocation (pre-challenge; baseline sample) and on days 1, 7, 14, 21 and 28 after allergen challenge. The 16S rRNA gene was amplified, sequenced and analysed. Staphylococcus spp. and Staphylococcus pseudintermedius were quantified with quantitative PCR (RT-qPCR).
RESULTS: Skin lesions developed in all dogs on the challenged sites. Differences in bacterial groups were observed on the challenged site over time. Relatively lower abundances of Fusobacteriaceae on Day 7, and, based on LEfSe, increased abundances of Corynebacteriaceae on Day 1, and Staphylococcaceae on days 7, 14 and 21, were observed on the challenged site, compared to the contralateral site. Results of RT-qPCR correlated with those of next-generation sequencing, with significantly increased numbers of Staphylococcus spp. and S. pseudintermedius on Day 21, and days 7 and 21 on the challenged site compared to the contralateral site, respectively.
CONCLUSIONS AND CLINICAL IMPORTANCE: This study demonstrates that an allergen challenge in sensitized dogs leads to bacterial dysbiosis with increased abundance of S. pseudintermedius at the site of lesion induction.
HYPOTHESIS/OBJECTIVES: This study evaluated temporal changes in the skin microbiota in a canine model of atopic dermatitis.
ANIMALS: Eight atopic dogs previously sensitized with house dust mites (HDM).
METHODS: The dogs were topically challenged on the right groin with HDM allergens. Swabs were collected from the challenged and the contralateral nonchallenged sites prior to provocation (pre-challenge; baseline sample) and on days 1, 7, 14, 21 and 28 after allergen challenge. The 16S rRNA gene was amplified, sequenced and analysed. Staphylococcus spp. and Staphylococcus pseudintermedius were quantified with quantitative PCR (RT-qPCR).
RESULTS: Skin lesions developed in all dogs on the challenged sites. Differences in bacterial groups were observed on the challenged site over time. Relatively lower abundances of Fusobacteriaceae on Day 7, and, based on LEfSe, increased abundances of Corynebacteriaceae on Day 1, and Staphylococcaceae on days 7, 14 and 21, were observed on the challenged site, compared to the contralateral site. Results of RT-qPCR correlated with those of next-generation sequencing, with significantly increased numbers of Staphylococcus spp. and S. pseudintermedius on Day 21, and days 7 and 21 on the challenged site compared to the contralateral site, respectively.
CONCLUSIONS AND CLINICAL IMPORTANCE: This study demonstrates that an allergen challenge in sensitized dogs leads to bacterial dysbiosis with increased abundance of S. pseudintermedius at the site of lesion induction.
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