Toll-like receptor 2 and facial motoneuron survival after facial nerve axotomy

NEUROSCIENCE LETTERS

卷:471

Article

Wainwright, Derek A.^1,2  Xin, Junping^1,2  Mesnard, Nichole A.^2,3  Sanders, Virginia M.⁴  Jones, Kathryn J.^1,2 

[1] Loyola Univ, Med Ctr, Dept Cell Biol Neurobiol & Anat, Maywood, IL 60153 USA

[2] Edward Hines Jr VA Hosp, Res & Dev Serv, Hines, IL 60141 USA

[3] Loyola Univ, Med Ctr, Neurosci Program, Maywood, IL 60153 USA

[4] Ohio State Univ, Dept Mol Virol Immunol & Med Genet, Columbus, OH 43210 USA

关键词: Neuroprotection;    PRR;    TLR2;    Facial motoneuron;    CNS;   

DOI  :  10.1016/j.neulet.2009.12.076

来源: Elsevier

【 摘 要 】

We have previously demonstrated that CD4(+) Th2 lymphocytes are required to rescue facial motoneuron (FMN) survival after facial nerve axotomy through interaction with peripheral antigen presenting cells, as well as CNS resident microglia. Furthermore, the innate immune molecule, toll-like receptor 2 (TLR2), has been implicated in the development of Th2-type immune responses and can be activated by intracellular components released by dead or dying cells. The role of TLR2 in the FMN response to axotomy was explored in this study, using a model of facial nerve axotomy at the stylomastoid foramen in the mouse, in which blood-brain-barrier (BBB) permeability does not occur. After facial nerve axotomy, TLR2 mRNA was significantly upregulated in the facial motor nucleus and co-immunofluorescence localized TLR2 to CD68(+) microglia, but not GFAP(+) astrocytes. Using TLR2-deficient (TLR2(-/-)) mice, it was determined that TLR2 does not affect FMN survival levels after axotomy. These data contribute to understanding the role of innate immunity after FMN death and may be relevant to motoneuron diseases, such as amyotrophic lateral sclerosis (ALS). (C) 2010 Elsevier Ireland Ltd. All rights reserved.

【 授权许可】

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