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The effects of the canine type C staphylococcal enterotoxin on the proliferation and cytokine expression by peripheral blood mononuclear cells from atopic and healthy dogs

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Authors

박정훈

Advisor
황철용
Major
수의과대학 수의학과
Issue Date
2014-08
Publisher
서울대학교 대학원
Keywords
atopic dermatitisstaphylococcal enterotoxin CPBMCsuperantigendog
Description
학위논문 (석사)-- 서울대학교 대학원 : 수의학과, 2014. 8. 황철용.
Abstract
Canine atopic dermatitis (AD) is defined as a genetically predisposed inflammatory and pruritic allergic skin disease associated with skin colonization by Staphylococcus pseudintermedius known to produce exotoxins with superantigen activity. Despite the high prevalence of the canine type C staphylococcal enterotoxin (SECcanine) in S. pseudintermedius of canine origin, its significance in S. pseudintermedius infections has not been well investigated. In this pilot study, the effects of SECcanine on proliferation and cytokine responses in canine peripheral blood mononuclear cells (PBMC) were investigated. PBMC from seven atopic dogs and six healthy dogs were stimulated with SECcanine and PBMC proliferation was demonstrated using WST-1 assay and the expression levels of IL-4, IL-5, IL-10, IL-13, IFN-γ, and TNF-α mRNAs in PBMC were quantified using a real-time PCR. Low concentration of SECcanine induced potent T cell proliferation in both atopic and normal dogs. PBMC of atopic dogs appear to be less substantial responses to SECcanine than those of the healthy controls. Of all the cytokines investigated in PBMC, the expression level of IL-4, IL-13, and IFN-γ mRNA was increased in both groups. Interestingly, the expression level of IFN-γ mRNA in atopic dogs was significantly higher than that in the healthy dogs. The results indicate that less proliferative response of PBMC than healthy dogs and Th1 like cytokine response occur in response to SECcanine in atopic dogs. These findings suggest that an infection of S. pseudintermedius producing SECcanine may play a role in aggravation factor of atopic dermatitis by reducing proliferation in T cells and immune response of canine AD by facilitating the development of Th1 cell dominated chronic lesion.
Language
English
URI
https://hdl.handle.net/10371/133719
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