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Published in: Molecular Pain 1/2011

Open Access 01-12-2011 | Research

Toll-like receptor 2 contributes to chemokine gene expression and macrophage infiltration in the dorsal root ganglia after peripheral nerve injury

Authors: Donghoon Kim, Byunghyun You, Hyoungsub Lim, Sung Joong Lee

Published in: Molecular Pain | Issue 1/2011

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Abstract

Background

We have previously reported that nerve injury-induced neuropathic pain is attenuated in toll-like receptor 2 (TLR2) knock-out mice. In these mice, inflammatory gene expression and spinal cord microglia actvation is compromised, whereas the effects in the dorsal root ganglia (DRG) have not been tested. In this study, we investigated the role of TLR2 in inflammatory responses in the DRG after peripheral nerve injury.

Results

L5 spinal nerve transection injury induced the expression of macrophage-attracting chemokines such as CCL2/MCP-1 and CCL3/MIP-1 and subsequent macrophage infiltration in the DRG of wild-type mice. In TLR2 knock-out mice, however, the induction of chemokine expression and macrophage infiltration following nerve injury were markedly reduced. Similarly, the induction of IL-1β and TNF-α expression in the DRG by spinal nerve injury was ameliorated in TLR2 knock-out mice. The reduced inflammatory response in the DRG was accompanied by attenuation of nerve injury-induced spontaneous pain hypersensitivity in TLR2 knock-out mice.

Conclusions

Our data show that TLR2 contributes to nerve injury-induced proinflammatory chemokine/cytokine gene expression and macrophage infiltration in the DRG, which may have relevance in the reduced pain hypersensitivity in TLR2 knock-out mice after spinal nerve injury.
Appendix
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Metadata
Title
Toll-like receptor 2 contributes to chemokine gene expression and macrophage infiltration in the dorsal root ganglia after peripheral nerve injury
Authors
Donghoon Kim
Byunghyun You
Hyoungsub Lim
Sung Joong Lee
Publication date
01-12-2011
Publisher
BioMed Central
Published in
Molecular Pain / Issue 1/2011
Electronic ISSN: 1744-8069
DOI
https://doi.org/10.1186/1744-8069-7-74

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