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HSV‐2 infection induces NF‐kB‐dependent cytokines in human cervical epithelial cells
Author(s) -
Li Hui,
Li Xiaoling,
Wei Yun,
Tan Yun,
Wu Xinxing
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.570.15
Subject(s) - herpes simplex virus , cytokine , biology , hsl and hsv , secretion , nf κb , virus , virology , immune system , cell culture , immunology , proinflammatory cytokine , interferon , inflammation , endocrinology , genetics
Herpes Simplex Virus type 2 (HSV‐2) is one of the most common sexually transmitted pathogen and can establish lifelong latency infection. Our previously studies have shown that HSV‐2 infection up‐regulates TLRs expression and activates NF‐kB signaling in human cervical epithelia (HCE) cells. In this study, we examined the cytokines production of HCE cells in response to HSV‐2. HCE cells were infected with HSV‐2 at 3 MOI and cultured for the certain period of times. The result showed that the secretion of IL‐6 and IFN‐beta increased dramatically after HSV‐2 infection and maintained high levels during the course of experiment . We asked whether or not the induction of cytokines requires NF‐¿B activity. To this end, we treated cells with Isohelenin and harvested the supernatants for ELISA assay. The presence of NF‐¿B inhibitor, Isohelenin significantly blocked the production of both IL‐6 and IFN‐beta in response to HSV‐2 compared to the untreated control. Thus, our data provide the direct evidence that the production of both IL‐6 and IFN‐beta induced by HSV‐2 in HCE cells was NF‐¿B dependent suggesting a critical role of NF‐¿B as a key regulator of cytokine production in response to HSV‐2 infection in its natural host cells. This work was supported by grant from the National Natural Science Foundation of China (No. 30500465, No. 30810103052)