Abstract
Toll-like receptors (TLR) recognize molecular structures associated with pathogens as well as host-derived components and initiate an inflammatory innate immune response. Microglia represent the resident immune host defense and are the major inflammatory cell type in the central nervous system (CNS). We show here that TLR2-deficient mice develop a decreased CNS injury compared to wild type mice in a model of focal cerebral ischemia. TLR2 mRNA is up-regulated in wild type mice during cerebral ischemia. In ischemic brains, TLR2 protein is expressed in lesion-associated microglia. Absence of TLR2 does not affect the recruitment of granulocytes to the infarct region. We conclude that TLR2 in microglia propagates stroke-induced CNS injury.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Brain / immunology*
-
Brain / metabolism
-
Brain / physiopathology
-
Brain Ischemia / genetics
-
Brain Ischemia / immunology*
-
Brain Ischemia / physiopathology
-
Cerebral Infarction / genetics
-
Cerebral Infarction / immunology*
-
Cerebral Infarction / physiopathology
-
Chemotaxis / genetics
-
Chemotaxis / immunology
-
Disease Models, Animal
-
Encephalitis / genetics
-
Encephalitis / immunology*
-
Encephalitis / physiopathology
-
Infarction, Middle Cerebral Artery / genetics
-
Infarction, Middle Cerebral Artery / immunology
-
Infarction, Middle Cerebral Artery / physiopathology
-
Male
-
Mice
-
Mice, Inbred C57BL
-
Mice, Knockout
-
Microglia / immunology
-
RNA, Messenger / metabolism
-
Toll-Like Receptor 2 / genetics*
-
Up-Regulation / genetics
-
Up-Regulation / immunology
Substances
-
RNA, Messenger
-
Tlr2 protein, mouse
-
Toll-Like Receptor 2