IL-10 overexpression attenuated expression of TNF-α and IL-1β activated by lipopolysaccharide in astrocytes.
Zhenghua He, Muzhang Xiao, Qulian Guo
Abstract
Zhenghua He, Muzhang Xiao, Qulian Guo
Abstract
OBJECTIVE: To investigate the intervention effect of lentivirus expressing human IL-10 (LV-hIL-10) on activated astrocytes. METHODS: DI TNC1 cell line was treated with different concentrations of lipopolysaccharide (LPS) and time points. The expression of proinflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukinb-1β (IL-1β) was detected by RT-PCR and ELISA. Moreover, the effect on the expression of proinflammatory cytokines TNF-α and IL-1β was analyzed in DI TNC1 cell lines infected with and without LV-hIL-10. RESULTS: The expression of TNF-α and IL-1β was increased in DI TNC1 induced by LPS. The expression of IL-10 was upregulated in DI TNC1 infected with LV-hIL-10. TNF-α and IL-1β were inhibited by IL-10 overexpression in DI TNC1 actived by LPS. CONCLUSION: DI TNC1 is activated by LPS and secretes proinflammatory cytokines TNF-α and IL-1β as immune-like cells, and these activation is inhibited by hIL-10 overexpression.
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OBJECTIVE: To investigate the intervention effect of lentivirus expressing human IL-10 (LV-hIL-10) on activated astrocytes. METHODS: DI TNC1 cell line was treated with different concentrations of lipopolysaccharide (LPS) and time points. The expression of proinflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukinb-1β (IL-1β) was detected by RT-PCR and ELISA. Moreover, the effect on the expression of proinflammatory cytokines TNF-α and IL-1β was analyzed in DI TNC1 cell lines infected with and without LV-hIL-10. RESULTS: The expression of TNF-α and IL-1β was increased in DI TNC1 induced by LPS. The expression of IL-10 was upregulated in DI TNC1 infected with LV-hIL-10. TNF-α and IL-1β were inhibited by IL-10 overexpression in DI TNC1 actived by LPS. CONCLUSION: DI TNC1 is activated by LPS and secretes proinflammatory cytokines TNF-α and IL-1β as immune-like cells, and these activation is inhibited by hIL-10 overexpression.
Key concepts: Proinflammatory cytokine, Lipopolysaccharide, Tumor necrosis factor alpha, Downregulation and upregulation, Immune system, Immunology, Cell culture, Molecular biology