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- Title
Traumatic brain injury induces macrophage subsets in the brain.
- Authors
Hsieh, Christine L.; Kim, Charles C.; Ryba, Bryan E.; Niemi, Erene C.; Bando, Jennifer K.; Locksley, Richard M.; Liu, Jialing; Nakamura, Mary C.; Seaman, William E.
- Abstract
Traumatic brain injury ( TBI) elicits innate inflammatory responses that can lead to secondary brain injury. To better understand the mechanisms involved in TBI-induced inflammation, we examined the nature of macrophages responding to TBI in mice. In this model, brain macrophages were increased >20-fold the day after injury and >77-fold 4 days after injury in the ipsilateral hemisphere compared with sham controls. TBI macrophage subsets were identified by using a reporter mouse strain ( YARG) that expresses e YFP from an internal ribosome entry site (IRES) inserted at the 3′ end of the gene for arginase-1 ( Arg1), a hallmark of alternatively activated ( M2) macrophages. One day after TBI, 21 ± 1.5% of ipsilateral brain macrophages expressed relatively high levels of Arg1 as detected by yellow fluorescent protein, and this subpopulation declined thereafter. Arg1+ cells localized with macrophages near the TBI lesion. Gene expression analysis of sorted Arg1 + and Arg1− brain macrophages revealed that both populations had profiles that included features of conventional M2 macrophages and classically activated ( M1) macrophages. The Arg1 + cells differed from Arg1− cells in multiple aspects, most notably in their chemokine repertoires. Thus, the macrophage response to TBI initially involves heterogeneous polarization toward at least two major subsets.
- Publication
European Journal of Immunology, 2013, Vol 43, Issue 8, p2010
- ISSN
0014-2980
- Publication type
Article
- DOI
10.1002/eji.201243084