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báo cáo hóa học: " Reactive oxygen species drive herpes simplex virus (HSV)-1-induced proinflammatory cytokine production by murine microglia"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Reactive oxygen species drive herpes simplex virus (HSV)-1-induced proinflammatory cytokine production by murine microglia | Hu et al. Journal of Neuroinflammation 2011 8 123 http www.jneuroinflammation.eom content 8 1 123 JJOURNAL1 OF. NEUROINFLAMMATION RESEARCH Open Access Reactive oxygen species drive herpes simplex virus HSV -1-induced proinflammatory cytokine production by murine microglia Shuxian Hu Wen S Sheng Scott J Schachtele and James R Lokensgard Abstract Background Production of reactive oxygen species ROS and proinflammatory cytokines by microglial cells in response to viral brain infection contributes to both pathogen clearance and neuronal damage. In the present study we examined the effect of herpes simplex virus HSV -1-induced NADPH oxidase-derived ROS in activating mitogen-activated protein kinases MAPKs as well as driving cytokine and chemokine expression in primary murine microglia. Methods Oxidation of 2 7 -dichlorodihydrofluorescin diacetate H2DCFDA was used to measure production of intracellular ROS in microglial cell cultures following viral infection. Virus-induced cytokine and chemokine mRNA and protein levels were assessed using real-time RT-PCR and ELISA respectively. Virus-induced phosphorylation of microglial p38 and p44 42 ERK1 2 MAPKs was visualized using Western Blot and levels of phospho-p38 were quantified using Fast Activated Cell-based ELISA FACE assay . Diphenyleneiodonium DPI and apocynin APO inhibitors of NADPH oxidases were used to investigate the role of virus-induced ROS in MAPK activation and cytokine as well as chemokine production. Results Levels of intracellular ROS were found to be highly elevated in primary murine microglial cells following infection with HSV and the majority of this virus-induced ROS was blocked following DPI and APO treatment. Correspondingly inhibition of NADPH oxidase also decreased virus-induced proinflammatory cytokine and chemokine production. In addition microglial p38 and p44 42 MAPKs were found to be phosphorylated in response to viral infection and this activation was also blocked by inhibitors of NADPH .