Temporal characterization of microglia/macrophage phenotypes in a mouse model of neonatal hypoxic-ischemic brain injury

Erkenstam, N, Smith, P, Fleiss, B, Nair, S, Sveden, P, Wang, W, Bostrom, M, Gressens, P, Hagberg, H, Brown, K, Savman, K and Mallard, C 2016, 'Temporal characterization of microglia/macrophage phenotypes in a mouse model of neonatal hypoxic-ischemic brain injury', Frontiers in Cellular Neuroscience, vol. 10, no. DEC2016, pp. 1-29.


Document type: Journal Article
Collection: Journal Articles

Title Temporal characterization of microglia/macrophage phenotypes in a mouse model of neonatal hypoxic-ischemic brain injury
Author(s) Erkenstam, N
Smith, P
Fleiss, B
Nair, S
Sveden, P
Wang, W
Bostrom, M
Gressens, P
Hagberg, H
Brown, K
Savman, K
Mallard, C
Year 2016
Journal name Frontiers in Cellular Neuroscience
Volume number 10
Issue number DEC2016
Start page 1
End page 29
Total pages 29
Publisher Frontiers Research Foundation
Abstract Immune cells display a high degree of phenotypic plasticity, which may facilitate their participation in both the progression and resolution of injury-induced inflammation. The purpose of this study was to investigate the temporal expression of genes associated with classical and alternative polarization phenotypes described for macrophages and to identify related cell populations in the brain following neonatal hypoxia-ischemia (HI). HI was induced in 9-day old mice and brain tissue was collected up to 7 days post-insult to investigate expression of genes associated with macrophage activation. Using cell-markers, CD86 (classic activation) and CD206 (alternative activation), we assessed temporal changes of CD11b+ cell populations in the brain and studied the protein expression of the immunomodulatory factor galectin-3 in these cells. HI induced a rapid regulation (6 h) of genes associated with both classical and alternative polarization phenotypes in the injured hemisphere. FACS analysis showed a marked increase in the number of CD11b+CD86+ cells at 24 h after HI (+3667%), which was coupled with a relative suppression of CD11b+CD206+ cells and cells that did not express neither CD86 nor CD206. The CD11b+CD206+ population was mixed with some cells also expressing CD86. Confocal microscopy confirmed that a subset of cells expressed both CD86 and CD206, particularly in injured gray and white matter. Protein concentration of galectin-3 was markedly increased mainly in the cell population lacking CD86 or CD206 in the injured hemisphere. These cells were predominantly resident microglia as very few galectin-3 positive cells co-localized with infiltrating myeloid cells in Lys-EGFP-ki mice after HI. In summary, HI was characterized by an early mixed gene response, but with a large expansion of mainly the CD86 positive population during the first day. However
Subject Innate Immunity
Neurology and Neuromuscular Diseases
Paediatrics
Keyword(s) Galectin-3
Microglia
Neuroinflammation
Perinatal brain injury
DOI - identifier 10.3389/fncel.2016.00286
Copyright notice © 2016 Hellström Erkenstam, Smith, Fleiss, Nair, Svedin, Wang, Boström, Gressens, Hagberg, Brown, Sävman and Mallard.
ISSN 1662-5102
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