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Temporal Changes in Cell Marker Expression and Cellular Infiltration in a Controlled Cortical Impact Model in Adult Male C57BL/6 Mice
Open accessAbstract
BACKGROUND: Traumatic injury to the central nervous system (CNS) triggers a robust inflammatory response that leads to axonal damage and secondary degeneration of spared tissue. In contrast, some immune responses have neuroprotective effects. However, detailed information regarding the dynamics of immune responses after traumatic CNS injury is still unavailable. METHODS: In the present study, changes in the immune cells present in the injured brain, spleen, and cervical lymph nodes (CLNs), which are draining lymphatic organs from the CNS, were analyzed after controlled cortical impact (CCI) by flow cytometry and immunohistochemistry. RESULTS: The number of neutrophils and macrophages that infiltrated the injured brain immediately increased 1 d post-injury and declined rapidly thereafter. In the injured brain, resident microglia showed a bimodal increase during the first week and in the chronic phase (≥3 weeks) after injury. Increase in the Iba-1(+) microglia/macrophages was observed around the injured site. Morphologic analysis showed that Iba-1(+) cells were round at 1 week, whereas those at 3 weeks were more ramified. Furthermore, CD86(+)/CD11b(+) M1-like microglia increased at 4 weeks after CCI, whereas CD206(+)/CD11b(+) M2-like microglia increased at 1 week. These results suggest that different subsets of microglia increased in the acute and chronic phases after CCI. Dendritic cells and T cells increased transiently within 1 week in the injured brain. In the CLNs and the spleen, T cells showed dynamic changes after CCI. In particular, the alteration in the number of T cells in the CLNs showed a similar pattern, with a 1-week delay, to that of microglia in the injured brain. CONCLUSION: The data from this study provide useful information on the dynamics of immune cells in CNS injuries.
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“Microglia associated with the long-term inflammatory phenotype following TBI are commonly defined as MHC-II/CD86/Cd11b positive, with upregulated expression of NOX24, Tlr4, Trem2, CD68, Clec7a, and Stat1, and higher expression of interferon- and immune-associated signaling genes [100,112,115,116].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [116]
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Metadata
- Authors
- Jin, X., Ishii, H., Bai, Z., Itokazu, T., & Yamashita, T.
- Affiliations
- Japan Science and Technology Agency (JP)
- Yunnan Agricultural University (CN)
- Corresponding author
- Yamashita, Toshihide
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2012-07-24
- Volume
- 7
- Issue
- 7
- Pages
- e41892
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3404031
- OpenAlex
- W2025828188
- Cited by
- 211
- References
- 48
- Citations by year
- 2026: 7 · 2025: 9 · 2024: 13 · 2023: 13 · 2022: 20 · 2021: 22 · 2020: 23 · 2019: 20 · 2018: 13 · 2017: 19 · 2016: 9 · 2015: 17 · 2014: 10 · 2013: 14 · 2012: 1
- FWCI
- 8.78
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Japan Science and Technology Agency (CREST)
- Core Research for Evolutional Science and Technology
- Topics
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
- Keywords
- controlled cortical impact, traumatic brain injury, microglia, macrophages, M1/M2 microglial polarization, dendritic cells, T cells, neutrophils, cervical lymph nodes, spleen, immune cell infiltration, neuroinflammation, Iba1, CD86, CD206
- MeSH terms
- Aging, Animals, Calcium-Binding Proteins, Cerebral Cortex, Dendritic Cells, Disease Models, Animal, Immunohistochemistry, Lymph Nodes, Macrophages, Male, Mice, Inbred C57BL, Microfilament Proteins, Neutrophils, Spleen, T-Lymphocytes, Time Factors, Biomarkers, Microglia, Mice
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