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Macrophage phagocytosis after spinal cord injury: when friends become foes

Van Broeckhoven, Jana, Sommer, Daniela, Dooley, Dearbhaile, Hendrix, Sven, Franssen, Aimée J P M·2021·Brain
DOI 10.1093/brain/awab250
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Abstract

After spinal cord injury, macrophages can exert either beneficial or detrimental effects depending on their phenotype. Aside from their critical role in inflammatory responses, macrophages are also specialized in the recognition, engulfment, and degradation of pathogens, apoptotic cells, and tissue debris. They promote remyelination and axonal regeneration by removing inhibitory myelin components and cellular debris. However, excessive intracellular presence of lipids and dysregulated intracellular lipid homeostasis result in the formation of foamy macrophages. These develop a pro-inflammatory phenotype that may contribute to further neurological decline. Additionally, myelin-activated macrophages play a crucial role in axonal dieback and retraction. Here, we review the opposing functional consequences of phagocytosis by macrophages in spinal cord injury, including remyelination and regeneration versus demyelination, degeneration, and axonal dieback. Furthermore, we discuss how targeting the phagocytic ability of macrophages may have therapeutic potential for the treatment of spinal cord injury.

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Metadata

Authors
Van Broeckhoven, J., Sommer, D., Dooley, D., Hendrix, S., & Franssen, A. J. P. M.
Affiliations
  • Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium
  • School of Medicine, Health Sciences Centre, University College Dublin, Belfield, Dublin 4, Ireland
ORCID
Hendrix, Sven
Venue
Brain
Publisher
Oxford University Press (OUP)
Published
2021-07-09
Volume
144
Issue
10
Pages
2933-2945
ISSN
  • 0006-8950
  • 1460-2156
DOI
10.1093/brain/awab250
Cited by
172
References
21
Language
en
Licence
academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
Funders
Fonds Wetenschappelijk Onderzoek—Vlaanderen (G067715N, G091518N, G0C2120N)

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