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Brain trauma is known to activate inflammatory cells via various chemokine signals although their interactions remain to be characterized. Mice deficient in  Ccl3 ,  Ccr2  or  Cxcl10  were compared with wildtype mice after controlled cortical impact injury. Expression of  Ccl3  in wildtypes was rapidly upregulated in resident, regularly spaced reactive microglia.  Ccl3 -deficiency enhanced endothelial expression of platelet selectin and invasion of peripheral inflammatory cells. Appearance of  Ccr2  transcripts, encoding the Ccl2 receptor, reflected invasion of lysozyme 2-expressing phagocytes and classical antigen-presenting dendritic cells expressing major histocompatibility complex class II.  Ccr2  also directed clustered plasmacytoid dendritic cells positive for the T-cell attracting chemokine  Cxcl10 . A reduction in  Ccr2  and dendritic cells was found in injured wildtype cortex after cyclophosphamide treatment resembling effects of  Ccr2 -deficiency. The findings demonstrate the feasibility to control inflammation in the injured brain by regulating chemokine-dependent pathways.

Interacting Chemokine Signals Regulate Dendritic Cells in Acute Brain Injury