Traumatic brain injury induces macrophage subsets in the brain.
Eur J Immunol, 2013/8;43(8):2010-22.
Hsieh CL[1], Kim CC, Ryba BE, Niemi EC, Bando JK, Locksley RM, Liu J, Nakamura MC, Seaman WE
Affiliations
PMID: 23630120DOI: 10.1002/eji.201243084
Impact factor: 6.688
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 eYFP 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.
Keywords: Alternative activation; Inflammation; Macrophage; Traumatic brain injury
MeSH terms
Animals; Arginase; Bacterial Proteins; Brain; Brain Injuries; Cell Movement; Chemokines; Gene Expression Profiling; Inflammation; Luminescent Proteins; Macrophage Activation; Macrophages; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Ribosomes
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