期刊
IMMUNOLOGY
卷 117, 期 2, 页码 167-176出版社
WILEY
DOI: 10.1111/j.1365-2567.2005.02275.x
关键词
corneal epithelium; herpes simplex virus 1; cytokines; Toll-like receptors; NF-kappa B
类别
资金
- NEI NIH HHS [EY06012, EY14080, R01 EY010869-12, R01 EY009169, R01 EY010869, R01 EY006012, EY09169, R01 EY014080-04, EY10869, R01 EY014080] Funding Source: Medline
Herpetic epithelial and stromal keratitis is a sight-threatening ocular infection. To study the role of the epithelium in the innate response to herpes simplex virus 1 (HSV-1) infection of the cornea, we used a telomerase-immortalized human corneal epithelial cell (HCEC) line, HUCL, and primary HCECs as a model and infected the cells with HSV-1 (KOS strain). HSV-1 infection of HCECs resulted in a two-phase activation of nuclear factor-kappaB (NF-kappa B), JNK and p38, with the first peak at 1-4 hr and a second peak at 8 hr. Concomitant with the first peak of activation, transcriptional expression of interleukin (IL)-6, IL-8, tumour necrosis factor (TNF)-alpha and interferon (IFN)-beta was rapidly induced in HSV-1-infected cells. HSV-1 infection also induced the production of IL-6, IL-8, and TNF-alpha in both HUCL cells and primary HCECs. Coincident with the second phase of NF-kappa B activation in HSV-1-infected HCECs, the expression of Toll-like receptor 7 (TLR7) was induced, whereas the level of TLR3 was greatly down-regulated. Thus, in response to HSV-1 infection, HCECs produce proinflammatory cytokines, leading to infiltration, and IFNs to enhance the antiviral activity in the cornea, probably through sequential activation of TLRs.
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