Cited by 366Neuroinflammation and Neurodegeneration MechanismsInflammasome and immune disordersNeurological Disease Mechanisms and Treatments

Microglia: Agents of the CNS Pro-Inflammatory Response

Open access
Rodríguez-Gómez, José A., Kavanagh, Edel, Engskog-Vlachos, Pinelopi, Engskog, Mikael K.R., Herrera, Antonio J., Espinosa-Oliva, Ana M., Joseph, Bertrand, Hajji, Nabil +2 more·2020·Cells

Abstract

The pro-inflammatory immune response driven by microglia is a key contributor to the pathogenesis of several neurodegenerative diseases. Though the research of microglia spans over a century, the last two decades have increased our understanding exponentially. Here, we discuss the phenotypic transformation from homeostatic microglia towards reactive microglia, initiated by specific ligand binding to pattern recognition receptors including toll-like receptor-4 (TLR4) or triggering receptors expressed on myeloid cells-2 (TREM2), as well as pro-inflammatory signaling pathways triggered such as the caspase-mediated immune response. Additionally, new research disciplines such as epigenetics and immunometabolism have provided us with a more holistic view of how changes in DNA methylation, microRNAs, and the metabolome may influence the pro-inflammatory response. This review aimed to discuss our current knowledge of pro-inflammatory microglia from different angles, including recent research highlights such as the role of exosomes in spreading neuroinflammation and emerging techniques in microglia research including positron emission tomography (PET) scanning and the use of human microglia generated from induced pluripotent stem cells (iPSCs). Finally, we also discuss current thoughts on the impact of pro-inflammatory microglia in neurodegenerative diseases.

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Crossref · 10.3390/cells9071717

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  • Activated microglia migrate to the site of damage via chemotaxis and release chemokines, pro- and anti-inflammatory cytokines, and other inflammatory mediators.

    “Activated microglia migrate to the site of damage via a process called chemotaxis and release chemokines (e.g., CCL2 and CXCL1), pro- and anti-inflammatory cytokines (e.g., IL-12, IL-10, TNF, TGF-β), and a variety of other inflammatory mediators [341].”

    From Revisiting the Pathogenesis of X-Linked Adrenoleukodystrophy (2025) · cites this paper as [341]

    Section 2.1 (page unavailable) describes microglial inflammatory signaling involving cytokines, including IL-12 and TNF, and chemokines, including CXCL1. Section 2 also lists other inflammatory factors, while section 5.3 discusses IL-10 expression in microglia. The passages found do not establish that activated microglia migrate to damage by chemotaxis or that they release TGF-β. (LLM, conf=0.87)

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Research works printed but not linked: 2

  1. [85]Carstens E. Akiyama T. Itch: Mechanisms and Treatment CRC Press/Taylor & Francis Boca Raton, FL, USA 2014 24830003
  2. [359]The National Academies of Sciences, Engineering and Medicine Biomarkers of Neuroinflammation—Proceedings of a Workshop The National Academies Press Washington, DC, USA 2018 28921942

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Authors
Rodríguez-Gómez, J. A., Kavanagh, E., Engskog-Vlachos, P., Engskog, M. K. R., Herrera, A. J., Espinosa-Oliva, A. M., Joseph, B., Hajji, N., Venero, J. L., & Burguillos, M. A.
Affiliations
  • Institute of Biomedicine of Seville (IBIS)-Hospital Universitario Virgen del Rocío/CSIC/University of Seville, 41012 Seville, Spain
  • Universidad de Sevilla (ES)
  • Institute of Environmental Medicine, Toxicology Unit, Karolinska Institute, 17177 Stockholm, Sweden
  • Uppsala University (SE)
  • Instituto de Biomedicina de Sevilla (ES)
  • Karolinska Institutet (SE)
  • Imperial College London (GB)
Venue
Cells
Publisher
MDPI AG
Published
2020-07-17
Volume
9
Issue
7
Pages
1717
ISSN
2073-4409 (ISSN-L)
OpenAlex
W3043443440
Cited by
365
References
414
Citations by year
2026: 40 · 2025: 80 · 2024: 69 · 2023: 54 · 2022: 71 · 2021: 41 · 2020: 9 · 2018: 1
FWCI
4.38
Type
journal article
Language
en
Open access
Locations
  • Cells (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (publishedVersion, cc-by-nc-nd)
  • RISalud Institutional Health Repository of Andalucía (submittedVersion, cc-by)
  • Uppsala University Publications (Uppsala University) (submittedVersion, other-oa)
  • DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Deposito de Investigacion Universidad de Sevilla (University of Seville) (submittedVersion, cc-by)
  • Spiral (Imperial College London) (submittedVersion, cc-by)
Funders
  • Ministerio de Ciencia, Innovación y Universidades /FEDER/UE (RTI2018-098645-B-100)
  • FEDER I+D+i-USE (US-1265062)
  • Ministerio de Economia y Competitividad (Programa Ramón y Cajal: RYC-2017-21804)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords
microglia, neuroinflammation, reactive microglia, homeostatic microglia, pattern recognition receptors, TLR4, TREM2, epigenetics, DNA methylation, microRNA, immunometabolism, exosomes, neurodegenerative diseases, iPSC-derived microglia
MeSH terms
Animals, Central Nervous System, Humans, Inflammation, Models, Biological, Microglia, Caspases, Epigenesis, Genetic

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