Introduction: Keratinocytes have an important role in the pathogenesis of atopic dermatitis (AD) through the production of numerous inflammatory signals and innate immune responses of the skin. We hypothesized that rhinovirus could induce pro-inflamma...
Introduction: Keratinocytes have an important role in the pathogenesis of atopic dermatitis (AD) through the production of numerous inflammatory signals and innate immune responses of the skin. We hypothesized that rhinovirus could induce pro-inflammatory cytokine, chemokine and cytokines which may drive Th2 immune response from human keratinocyte. We evaluated mRNA expression of cytokines from human keratinocytes infected by human rhinovirus (HRV) 16 and 1B. Materials and Methods: Established lines of human immortalized keratinocytes (HaCaT cell line) were infected with HRV 16 and 1B at a multiplicity of infection (MOI) equal to 1-2. mRNA expressions of IL-8, IL-25, IL-33 TSLP, RANTES, TNF-α, and IFN-β were analyzed using real time quantitative polymerase chain reaction (RT-qPCR) at 6, 16, and 24 hours after HRV 16 infection and 6, 16, 24 and 48 hours after HRV 1B infection. Results: mRNA expression of IL-8, IL-25, TSLP, and IFN-β by HRV 16 and 1B, IL-33 and TNF-α by HRV 16 were higher than those in non-infected control cells. mRNA expressions of RANTES by HRV 16 and 1B also showed increased trends. Meaningful mRNA expression patterns of IL-25, TSLP, RANTES, TNF-α and IFN-β occurred earlier in stimulated HRV 16 than in HRV 1B. Conclusions: This study suggests that rhinovirus may play a role in modulating the Th2 mediated inflammation in human keratinocytes. Keywords: keratinocyte, Rhinovirus, cytokine