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J Neuroinflammation. 2007 Apr 30;4:11.

Toll-like receptor 2 signaling is a mediator of apoptosis in herpes simplex virus-infected microglia.

Author information

  • 1Center for Infectious Diseases and Microbiology Translational Research, University of Minnesota Medical School, Minneapolis, MN 55455, USA. arava001@umn.edu <arava001@umn.edu>

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 apoptosis-specific microarrays. The data obtained from microarray analysis were then validated using quantitative real-time PCR assays.

RESULTS:

HSV infection induced apoptotic cell death in microglial cells from wild-type as well as TLR2 cells. However, the cell death at 24 h p.i. was markedly lower in knockout cells. Furthermore, microarray analyses clearly showed that the expression of pro-apoptotic genes was down-regulated at the time when wild-type cells were actively undergoing apoptosis, indicating a differential response to HSV in cells with or without TLR2.

CONCLUSION:

We demonstrate here that HSV induces an apoptotic response in microglial cells which is mediated through TLR2 signaling.

PMID:
17470292
[PubMed - indexed for MEDLINE]
PMCID:
PMC1866225
Free PMC Article
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