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- W2078540140 abstract "We have established an in vitro HSV-2 acute infection model with Human cervical epithelial (HCE cells, the primary target and natural host cells for HSV-2) to investigate the role of TLRs-mediated innate immune response to HSV-2. In current study, we found that HSV-2 infection induced activity of NF-kB reporter and expression of cytokines are TLR4-dependent using approaches with shRNA and TLR4 antagonist. Knockdown experiments demonstrated that the adaptor molecules MyD88 and Mal of the TLRs signaling pathway are required in the HSV-2 induced TLR4-dependent NF-kB activation in HCE cells. Western blot assay suggested that knockdown of TLR4 decreased the phosphorylation of IRAK1 and inhibitor of NF-kB (IkB-α) upon HSV-2 infection. Finally, decreased expression of either TLR4 or MyD88/Mal alone or both significantly abolished productions of IL-6 and IFN-β by ELISA analysis. Taken together, our results from the in vitro infection model reveal for the first time that there exists the pathway via TLR4-Mal/MyD88-IRAK1-NF-kB axis in human cervical epithelial cells in response to HSV-2 infection." @default.
- W2078540140 created "2016-06-24" @default.
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- W2078540140 date "2013-11-20" @default.
- W2078540140 modified "2023-10-11" @default.
- W2078540140 title "TLR4-MyD88/Mal-NF-kB Axis Is Involved in Infection of HSV-2 in Human Cervical Epithelial Cells" @default.
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- W2078540140 doi "https://doi.org/10.1371/journal.pone.0080327" @default.
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