Interleukin 4 Reduces Brain Hyperexcitability after Traumatic Injury by Downregulating TNF-α, Upregulating IL-10/TGF-β, and Potential Directing Macrophage/Microglia to the M2 Anti-inflammatory Phenotype

Radpour, Mozhdeh; Khoshkroodian, Bahar; Asgari, Tara; Pourbadie, Hamid Gholami; Sayyah, Mohammad

doi:10.1007/s10753-023-01843-0

Cited by 13 publications

(1 citation statement)

References 85 publications

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“…increase the infiltration of monocytes, promote the secretion of endothelial cell adhesion factors, and induce BBB damage [ 28 ]. The upregulation of anti-inflammatory cytokines (IL-10 and TGF-β) by IL-4 administration can regulate post-traumatic neuroinflammation and inhibit cell apoptosis [ 29 ]. In this study, we found that the expression time of each immune/inflammatory cytokine was not entirely consistent after TBI.…”

Section: Discussionmentioning

confidence: 99%

Progesterone induces neuroprotection associated with immune/inflammatory modulation in experimental traumatic brain injury

Zhou,

Li,

Peng

et al. 2024

NeuroReport

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An imbalance of immune/inflammatory reactions aggravates secondary brain injury after traumatic brain injury (TBI) and can deteriorate clinical prognosis. So far, not enough therapeutic avenues have been found to prevent such an imbalance in the clinical setting. Progesterone has been shown to regulate immune/inflammatory reactions in many diseases and conveys a potential protective role in TBI. This study was designed to investigate the neuroprotective effects of progesterone associated with immune/inflammatory modulation in experimental TBI. A TBI model in adult male C57BL/6J mice was created using a controlled contusion instrument. After injury, the mice received consecutive progesterone therapy (8 mg/kg per day, i.p.) until euthanized. Neurological deficits were assessed via Morris water maze test. Brain edema was measured via the dry–wet weight method. Immunohistochemical staining and flow cytometry were used to examine the numbers of immune/inflammatory cells, including IBA-1+ microglia, myeloperoxidase+ neutrophils, and regulatory T cells (Tregs). ELISA was used to detect the concentrations of IL-1β, TNF-α, IL-10, and TGF-β. Our data showed that progesterone therapy significantly improved neurological deficits and brain edema in experimental TBI, remarkably increased regulatory T cell numbers in the spleen, and dramatically reduced the activation and infiltration of inflammatory cells (microglia and neutrophils) in injured brain tissue. In addition, progesterone therapy decreased the expression of the pro-inflammatory cytokines IL-1β and TNF-α but increased the expression of the anti-inflammatory cytokine IL-10 after TBI. These findings suggest that progesterone administration could be used to regulate immune/inflammatory reactions and improve outcomes in TBI.

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Section: Discussionmentioning

confidence: 99%

Progesterone induces neuroprotection associated with immune/inflammatory modulation in experimental traumatic brain injury

Zhou,

Li,

Peng

et al. 2024

NeuroReport

View full text Add to dashboard Cite

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Research progress on the role of inflammatory mediators in the pathogenesis of epilepsy

Yu,

Sun

2024

Ibrain

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Epilepsy is an abnormal neurologic disorder distinguished by the recurrent manifestation of seizures, and the precise underlying mechanisms for its development and progression remain uncertain. In recent years, the hypothesis that inflammatory mediators and corresponding pathways contribute to seizures has been supported by experimental results. The potential involvement of neuroinflammation in the development of epilepsy has garnered growing interest. This review centers attention on the involvement of inflammatory mediators in the emergence and progression of epilepsy within recent years, focusing on both clinical research and animal models, to enhance comprehension of the intricate interplay between brain inflammation and epileptogenesis.

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Crosstalk Among Glial Cells in the Blood–Brain Barrier Injury After Ischemic Stroke

Lu,

Wen

2024

Mol Neurobiol

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Interleukin 4 Reduces Brain Hyperexcitability after Traumatic Injury by Downregulating TNF-α, Upregulating IL-10/TGF-β, and Potential Directing Macrophage/Microglia to the M2 Anti-inflammatory Phenotype

Cited by 13 publications

References 85 publications

Progesterone induces neuroprotection associated with immune/inflammatory modulation in experimental traumatic brain injury

Progesterone induces neuroprotection associated with immune/inflammatory modulation in experimental traumatic brain injury

Research progress on the role of inflammatory mediators in the pathogenesis of epilepsy

Crosstalk Among Glial Cells in the Blood–Brain Barrier Injury After Ischemic Stroke

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