Augmentation of CCL17 and CCL28 gene expression by TNF-alpha, IL-1beta, or IFN-gamma in cultured canine keratinocytes
Shibata S, Maeda S, Maeda S, Chimura N, Kondo N, Fukata T.
The United Graduate School of Veterinary Sciences, Gifu University, 1-1 Yanagido, Gifu
Research in Veterinary Science
Keratinocytes produce inflammatory mediators that are involved in the pathogenesis of skin disorders such as atopic dermatitis (AD). In particular, the CC chemokines, thymus and activation regulated chemokine (TARC)/CCL17 and mucosae-associated epithelial chemokine (MEC)/CCL28 are considered to play an important role in the lesional infiltration of lymphocytes in canine AD. However, there have been no reports on the regulatory mechanisms of CCL17 and CCL28 transcription in canine keratinocytes. In this study, we investigated whether CCL17 and CCL28 transcription in cultured keratinocytes is induced by TNF-alpha, IL-1beta, or IFN-gamma. It was found that CCL17 mRNA transcription is augmented by TNF-alpha only, whereas the CCL28 mRNA level could be increased by TNF-alpha, IL-1beta, or IFN-gamma. The present study suggests that pro-inflammatory cytokines are important inducing factors for the production of CCL17 and CCL28 in the lesional skin of dogs with AD.
Detection of CCL17 and CCL28 mRNA by RT-PCR, detection of CCL17 and CCL28 mRNA by RT-PCR. Comparison of CPEK to primary cells, concluding that CPEK „would be a useful experimental tool for investigating the mechanism of CCL17 and CCL28 production”.