tailieunhanh - báo cáo hóa học: " Toll-like receptor 2 signaling is a mediator of apoptosis in herpes simplex virus-infected 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: Toll-like receptor 2 signaling is a mediator of apoptosis in herpes simplex virus-infected microglia | Journal of Neuroinflammation BioMed Central Research Open Access Toll-like receptor 2 signaling is a mediator of apoptosis in herpes simplex virus-infected microglia Rajagopal N Aravalli Shuxian Hu and James R Lokensgard Address Center for Infectious Diseases and Microbiology Translational Research University of Minnesota Medical School Minneapolis MN 55455 USA Email Rajagopal N Aravalli - arava001@ Shuxian Hu - huxxx001@ James R Lokensgard - loken006@ Corresponding author Published 30 April 2007 Received 15 February 2007 Journal of Neuroinflammation 2007 4 11 doi 1742-2094-4-11 Accepted 30 Apnl 2007 This article is available from http content 4 1 11 2007 Aravalli et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Information regarding the response of brain cells to infection with herpes simplex virus HSV -1 is needed for a complete understanding of viral neuropathogenesis. We have recently demonstrated that microglial cells respond to HSV infection by producing a number of proinflammatory cytokines and chemokines through a mechanism involving Toll-like receptor 2 TLR2 . Following this cytokine burst microglial cells rapidly undergo cell death by apoptosis. We hypothesized that TLR2 signaling might mediate the cell death process as well. Methods To test this hypothesis we investigated HSV-induced cell death of microglia obtained from both wild-type and TLR2- - mice. Cell death was studied by oligonucleosomal ELISA and TUNEL staining and the mechanisms of apoptosis were further analyzed using murine apoptosisspecific microarrays. The data obtained from microarray analysis were then validated using quantitative real-time PCR assays. Results HSV .

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