TY - JOUR
T1 - Toll-like receptor 2 and facial motoneuron survival after facial nerve axotomy
AU - Wainwright, Derek A.
AU - Xin, Junping
AU - Mesnard, Nichole A.
AU - Sanders, Virginia M.
AU - Jones, Kathryn J.
N1 - Funding Information:
This work was supported by NIH grant NS40433 (KJJ and VMS) and the Les Turner ALS Foundation (DAW and KJJ).
PY - 2010/2/26
Y1 - 2010/2/26
N2 - 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).
AB - 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).
KW - CNS
KW - Facial motoneuron
KW - Neuroprotection
KW - PRR
KW - TLR2
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U2 - 10.1016/j.neulet.2009.12.076
DO - 10.1016/j.neulet.2009.12.076
M3 - Article
C2 - 20056129
AN - SCOPUS:75749083947
SN - 0304-3940
VL - 471
SP - 10
EP - 14
JO - Neuroscience Letters
JF - Neuroscience Letters
IS - 1
ER -