Recent studies indicate that several Toll-like receptors (TLRs) are implicated in recognizing viral structures and instigating immune responses against viral infections. The aim of this study is to examine the expression of TLRs and proinflammatory cytokines in viral skin diseases such as verruca vulgaris (VV) and molluscum contagiosum (MC). Reverse transcription-polymerase chain reaction and immunostaining of skin samples were performed to determine the expression of specific antiviral and proinflammatory cytokines as well as 5 TLRs (TLR2, 3, 4, 7, and 9). In normal human skin, TLR2, 4, and 7 mRNA was constitutively expressed, whereas little TLR3 and 9 mRNA was detected. Compared to normal skin (NS), TLR3 and 9 mRNA was clearly expressed in VV and MC specimens. Likewise, immunohistochemistry indicated that keratinocytes in NS constitutively expressed TLR2, 4, and 7; however, TLR3 was rarely detected and TLR9 was only weakly expressed, whereas 5 TLRs were all strongly expressed on the epidermal keratinocytes of VV and MC lesions. In addition, the mRNA expression of IFN-β and TNF-α was upregulated in the VV and MC samples. Immunohistochemistry indicated that IFN-β and TNF-α were predominately localized in the granular layer in the VV lesions and adjacent to the MC bodies. Our results indicated that VV and MC skin lesions expressed TLR3 and 9 in addition to IFN-β and TNF-α. These viral-induced proinflammatory cytokines may play a pivotal role in cutaneous innate immune responses.

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Tannic acids (TAs) are believed to be the key active components in plants, and are believed to be responsible for their anti-inflammatory, anti-viral effects and chemoprevention of cancer. However, the molecular mechanisms for the action of TA are unclear. This study examined the effects of TA on cutaneous inflammation with a human keratinocyte cell line (HaCaT). Interleukin-18 (IL-18) has multiple effects upon various cells involved in inflammatory response. In this study, the IL-18 mRNA expression and protein levels were reduced by a TA pretreatment. UV radiation can trigger the induction of the p38 mitogen-activated protein kinase (MAPK)-dependent signalling cascade. Immunoprecipitation and Western blot analysis was performed to determine if TA regulate the MAPK signalling pathway. TA significantly inhibited the activation of p38 MAPK and extracellular signal-regulated protein kinases. Moreover, TA-inhibited UVB enhanced the expression of the inflammatory mediators, IL-1, IL-6, tumor necrotic factor-alpha, cyclooxygenase-2 and prostaglandin E(2) in UVB-irradiated HaCaT cells. The topical application of TA on mouse skin treated with UVB irradiation has shown that TA inhibited the formation of erythema. These findings suggest that TA has significant anti-inflammatory effects on the UVB-induced response on the skin and may be a candidate natural compound for the regulation of cutaneous inflammation.