Transcription of thymic stromal lymphopoietin via Toll-like receptor 2 in canine keratinocytes: a possible association of Staphylococcus spp. in the deterioration of allergic inflammation in canine atopic dermatitis

• Published in: Veterinary dermatology 2016-06, Vol.27 (3), p.184-e46
• Main Authors: Sakamoto, Mayu, Asahina, Ryota, Kamishina, Hiroaki, Maeda, Sadatoshi
• Format: Article
• Language: English
• Subjects: Animals; Cytokines - genetics; Cytokines - metabolism; Dermatitis, Atopic - complications; Dermatitis, Atopic - metabolism; Dermatitis, Atopic - veterinary; Dog Diseases - etiology; Dog Diseases - metabolism; Dog Diseases - pathology; Dogs; Gene Expression Regulation - immunology; Hypersensitivity - veterinary; Inflammation - metabolism; Inflammation - veterinary; Keratinocytes - metabolism; Staphylococcal Skin Infections - complications; Staphylococcal Skin Infections - metabolism; Staphylococcal Skin Infections - veterinary; Staphylococcus; Toll-Like Receptor 2 - genetics; Toll-Like Receptor 2 - metabolism
• ISSN: 0959-4493; 1365-3164
• DOI: 10.1111/vde.12301

Background Colonization, overgrowth and subsequent infection by Staphylococcus spp. is frequently observed in canine atopic dermatitis (CAD), where it contributes to the intensity of cutaneous inflammation. The mechanisms by which staphylococci contribute to the pathogenesis of CAD are unclear. Studies suggest that thymic stromal lymphopoietin (TSLP), a cytokine induced by a cell wall component of Staphylococcus spp., may play a critical role in Th2 responses including the pathogenesis of CAD. Hypothesis/Objective To determine if synthetic triacylated lipopeptide (TLR1/2 ligand), a cell wall component of Staphylococcus spp., induces the transcription of TSLP via TLR2 in canine keratinocytes. Methods Transcription of TSLP was quantified in a canine keratinocyte cell line after stimulation with synthetic triacylated lipopeptide, and again after inhibition of TLR2 by a targeted small interfering RNA. Results The transcription of TSLP was enhanced 6 h after stimulation with the synthetic triacylated lipopeptide; it was completely suppressed by knockdown of TLR2. Conclusions and clinical importance The results demonstrated that a synthetic cell wall component of Staphylococcus spp. induced transcription of TSLP via TLR2 in canine keratinocytes. Additional studies will be required to investigate whether Staphylococcus spp. contributes to Th2 responses in CAD through TLR2‐mediated TSLP production. Résumé Contexte La colonisation, la multiplication et l'infection résultante liée à Staphylococcus spp est fréquemment observée dans la dermatite atopique canine (DAC) pour laquelle elle contribue à l'intensité de l'inflammation cutanée. Les mécanismes par lesquels les staphylocoques contribuent à la pathogénie de la DAC sont obscurs. Des études suggèrent que la TSLP (thymic stromal lymphopoietin), une cytokine induite par un composant de la paroi cellulaire de Staphylococcus spp., pourrait jouer un rôle critique dans les réponses Th2 comprenant la pathogénie de la DAC. Hypothèses/Objectifs Déterminer si un lipopeptide triacétylé synthétic (TLR1/2 ligand), un composant de la paroi cellulaire de Staphylococcus spp., induit la transcription de TSLP via TLR2 dans les kératinocytes canins. Méthodes La transcription de TSLP a été quantifiée dans une ligne cellulaire de kératinocytes après stimulation par un lipopeptide triacétylé synthétique, et après inhibition de TLR2 par un petit ARN ciblé. Résultats La transcription de TSLP a été augmentée 6h après stimulation avec le li