Cited by 34Inflammasome and immune disordersMultiple Sclerosis Research StudiesNeuroinflammation and Neurodegeneration Mechanisms

Reactive astrocytes and perivascular macrophages express NLRP 3 inflammasome in active demyelinating lesions of multiple sclerosis and necrotic lesions of neuromyelitis optica and cerebral infarction

Kawana, Natsuki, Yamamoto, Yoji, Ishida, Tsuyoshi, Saito, Yuko, Konno, Hidehiko, Arima, Kunimasa, Satoh, Jun‐ichi·2013·Clinical and Experimental Neuroimmunology

Abstract

Abstract Objective Inflammasome, activated by pathogen‐derived and host‐derived danger signals, constitutes a multimolecular signaling complex that serves as a platform for caspase‐1 (CASP1) activation and interleukin‐1β (IL‐1B) maturation. Mice deficient for NLRP3 inflammasome components are resistant to experimental autoimmune encephalomyelitis (EAE), suggesting a pro‐inflammatory role of NLRP3 inflammasome. However, at present, a pathological role of NLRP3 inflammasome in multiple sclerosis (MS) brains remains unknown. Methods We studied the expression of NLRP3 inflammasome components in active demyelinating lesions of MS by immunohistochemistry. Results Reactive astrocytes and perivascular macrophages expressed all three components of NLRP3 inflammasome – NLRP3, ASC and CASP1 – along with IL‐1B in active demyelinating lesions of MS, active necrotic lesions of neuromyelitis optica (NMO) and acute necrotic lesions of cerebral infarction. In contrast, the levels of expression of NLRP3, ASC, CASP1, and IL‐1B were greatly reduced in chronic inactive lesions of MS and gliotic lesions of cerebral infarction. Furthermore, the great majority of ramified and amoeboid microglia did not express NLRP3 in active and inactive MS lesions. Conclusions NLRP3 inflammasome could be activated chiefly in reactive astrocytes and infiltrating macrophages under the condition of active destruction of brain tissues that potentially provides a danger signal.

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Crossref · 10.1111/cen3.12068

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  • Inflammasome signaling in the CNS has been reported in microglia, astrocytes, perivascular brain-resident macrophages, oligodendrocytes, endothelial cells, and neurons.

    “Inflammasome signaling in the CNS has also been reported in the microglia, the brain’s critical innate immune cells (206), in astrocytes (207), perivascular brain-resident macrophages (208), oligodendrocytes (209), endothelial cells (210), as well as in neurons (211).”

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Authors
Kawana, N., Yamamoto, Y., Ishida, T., Saito, Y., Konno, H., Arima, K., & Satoh, J.
Affiliations
  • Meiji Pharmaceutical University (JP)
  • Kohnodai Hospital, National Center for Global Health and Medicine (JP)
  • National Center of Neurology and Psychiatry (JP)
  • Sendai Nishitaga National Hospital (JP)
Corresponding author
Satoh, Jun‐ichi
Venue
Clinical and Experimental Neuroimmunology
Publisher
Wiley
Published
2013-11-11
Volume
4
Issue
3
Pages
296-304
ISSN
1759-1961 (ISSN-L)
OpenAlex
W2092994936
Cited by
34
References
38
Citations by year
2025: 3 · 2024: 2 · 2023: 6 · 2022: 2 · 2021: 3 · 2020: 5 · 2019: 3 · 2017: 2 · 2016: 4 · 2015: 2 · 2014: 1 · 2013: 1
FWCI
1.19
Type
journal article
Language
en
Open access
closed
Locations
Clinical and Experimental Neuroimmunology (publishedVersion)
Funders
Japan Society for the Promotion of Science (25430054)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
NLRP3 inflammasome, multiple sclerosis, neuromyelitis optica, cerebral infarction, reactive astrocytes, perivascular macrophages, caspase-1, IL-1β, ASC, demyelinating lesions, necrotic lesions, microglia, neuroinflammation, damage-associated molecular patterns

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