Neuroinflammation and M2 microglia: the good, the bad, and the inflamed
By Jonathan D. Cherry, J. Olschowka, M. O’Banion. Journal of Neuroinflammation, 2014
1,598 citations recorded by the source corpus.
The concept of multiple macrophage activation states is not new. However, extending this idea to resident tissue macrophages, like microglia, has gained increased interest in recent years. Unfortunately, the research on peripheral macrophage polarization does not necessarily translate accurately to their central nervous system (CNS) counterparts. Even though pro- and anti-inflammatory cytokines can polarize microglia to distinct activation states, the specific functions of these states is still an area of intense debate. This review examines the multiple possible activation states microglia can be polarized to. This is followed by a detailed description of microglial polarization and the functional relevance of this process in both acute and chronic CNS disease models described in the literature. Particular attention is given to utilizing M2 microglial polarization as a potential therapeutic option in treating diseases.
Subfields: Immunology, Molecular Biology, Neurology
View Paper: https://www.semanticscholar.org/paper/e75a530e182cbacebb7bbb9d30d6b81723e41b09
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Citations in the corpus
- Microglial M1/M2 polarization and metabolic states (2016, background): “As in macrophages, microglia in the surveillance state are likely to rely on oxidative phosphorylation metabolism (Cherry et al., 2014b).”
- Irradiation in a flash: Unique sparing of memory in mice after whole brain irradiation with dose rates above 100Gy/s. (2017, background): “Both neuroinflammation [27] and synaptic changes [28] are known to interfere with cognitive functions after WBI and could be differentially induced after Flash WBI.”
- Microglia Polarization From M1 to M2 in Neurodegenerative Diseases (2022, methodology): “AD patients have a high expression of NADPH oxidase in microglia (Choi et al., 2012), and inhibiting NADPH oxidase drives microglia phenotype from M1 to M2, which is a potential therapeutic approach in AD (Choi et al., 2012).”
- The Biology of Regeneration Failure and Success After Spinal Cord Injury. (2018, background): “Successive axonal dieback (49, 171) due to aggressive macrophage activity (70, 201) and demyelination (41) also occur in the proximal segment which, in turn, may contribute to the list of factors that limit collateral sprouting (75).”
- The biphasic function of microglia in ischemic stroke (2017, neutral): “The functions of classically activated microglia are to present antigens and kill intracellular pathogens to maintain environmental homeostasis (Cherry et al., 2014).”