Role of Macrophages in Status Epilepticus Predisposing to Alzheimer’s Disease

Song, Shasha; Chen, Jingjiong; Xiao, Ping; Duan, Hao; Zhou, Yajun; Feng, Wenfang; Wang, Hongmei; Zhao, Yang; Geng, Zhi

doi:10.3233/jad-190994

Cited by 4 publications

(3 citation statements)

References 15 publications

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“…CD11c is an integrin alpha X chain protein, functioning in the adherence of neutrophils and monocytes to stimulated endothelium cells, and in the phagocytosis of complement coated particles. CD11c is a marker for monocytes and macrophages, but also expressed in dendritic cells [12,13]. F4/80 is EGF-like modulecontaining mucin-like hormone receptor-like 1 (EMR1), a member of the adhesion G protein-coupled receptor family.…”

Section: Discussionmentioning

confidence: 99%

Alveolar macrophage - derived exosomes modulate severity and outcome of acute lung injury

Bao

et al. 2020

Aging

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Severe acute lung injury (ALI) can cause death, and the survivals may develop acute respiratory distress syndrome (ARDS) due to fibrotic repair of the lung. Alveolar macrophages play a demonstrative role during the pathogenesis of ALI, and the timing and degree of differentially polarization of macrophages determine the severity of disease and outcome. Exosomes are important mediators of cellular communication and play critical roles during macrophage differentiation, proliferation and function. Nevertheless, the exact effects of alveolar macrophage-derived exosomes on ALI remain unknow. Here, we used lipopolysaccharide (LPS) to induce ALI in mice and analyzed the exosome population in bronchoalveolar lavage fluid (BALF) from macrophages, neutrophils and epithelial cells at different time points after treatment. Our data showed that macrophages were the major secretors for early secreted pro-inflammatory cytokines in the BALF-exosomes, which likely activated neutrophils to produce a variety of pro-inflammatory cytokines and IL-10. IL-10 by neutrophils in BALF-exosomes likely in turn polarized macrophages to M2c, which may be responsible for post-ALI fibrosis. Our study thus reveals a previous non-acknowledged role of BALF-exosomes as a mediator of inflammatory response and cell crosstalk during ALI.

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Section: Discussionmentioning

confidence: 99%

Alveolar macrophage - derived exosomes modulate severity and outcome of acute lung injury

Bao

et al. 2020

Aging

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“…The pro-inflammatory properties of HMGB1 are activated by binding to receptors such as toll-like receptor 4 (TLR 4), thereby mediating nuclear factor-κB (NF-κB) or other pathways ( 27 ). In both animal models and human patients, HMGB1 is actively expressed in epileptic tissues ( 2 , 28 ). TLR4 belongs to the TLR family and is expressed in microglia, oligodendrocytes, and astrocytes within the central nervous system ( 29 ).…”

Section: Introductionmentioning

confidence: 99%

“…Rather, they mitigate inflammatory responses by competing with TLRs for ligands ( 35 ). HMGB1 and TLR4 can quickly trigger the activation of pro-inflammatory signaling pathways, disrupt the blood-brain barrier (BBB), and increase the severity of seizures ( 7 , 21 , 28 , 36 ). Multiple studies in animal models of epilepsy have shown that activating the HMGB1/TLR4 signaling pathway leads to a marked increase in the frequency of seizures ( 7 , 27 , 37 , 38 ).…”

Section: Introductionmentioning

confidence: 99%

Investigation of Correlation between Resistance to Diazepam and Expression of Inflammatory Markers in The Peripheral Blood of Patients with Status of Epilepticus

Mahama,

Louisa,

Octaviana

et al. 2024

ama

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Objective. This study investigated several inflammatory markers’ gene and protein expression in status epilepticus (SE) and their correlation with diazepam resistance. Materials and Methods. Peripheral blood samples were collected from 18 adult patients with SE in Cipto Mangunkusumo Central Hospital, consisting of 12 diazepam-responsive and six diazepam-resistant samples, within 72 hours of the onset of the seizure. We collected baseline demographic and clinical data from each subject. Peripheral blood mononuclear cells (PBMCs) were isolated, cultured, stimulated with lipopolysaccharide (LPS) 1 mg/ml, and harvested for RNA isolation. The RNA was used to determine the expression of Human Mobility Group Box 1 (HMGB1), Inter- leukin-6 (IL-6), IL-10, Toll-like Receptor 4 (TLR4), and Glial fibrillary acidic protein (GFAP). In addition, we performed serum protein assay of HMGB1, IL-6, IL-10, TLR4, and GFAP to compare with gene expression. Results. We found a significant differ- ence between the responsive and resistant groups for serum HMGB1 and IL-6 concentration. The mRNA expression of HMGB1 and IL-6 was significantly higher in LPS-stimulated samples in the responsive but not in the resistant groups. The ratio of IL-6 to IL-10 showed a significant difference between LPS and control in the responsive group. Diazepam response was significantly correlated with seizure duration and serum protein concentration of HMGB1. Conclusion. HMGB1 was highly expressed in the resistant group and strongly correlated with diazepam response, and there was a significant increase in HMGB1 mRNA expres- sion in response to LPS stimulation. These findings suggest that targeting HMGB1 may be a promising therapeutic strategy and that HMGB1 levels could be a valuable biomarker for predicting diazepam resistance in SE.

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Oxymatrine blocks the NLRP3 inflammasome pathway, partly downregulating the inflammatory responses of M1 macrophages differentiated from THP-1 monocytes

Zhang

Liu

Zhao

et al. 2023

Biochemistry and Biophysics Reports

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Role of Macrophages in Status Epilepticus Predisposing to Alzheimer’s Disease

Cited by 4 publications

References 15 publications

Alveolar macrophage - derived exosomes modulate severity and outcome of acute lung injury

Alveolar macrophage - derived exosomes modulate severity and outcome of acute lung injury

Investigation of Correlation between Resistance to Diazepam and Expression of Inflammatory Markers in The Peripheral Blood of Patients with Status of Epilepticus

Oxymatrine blocks the NLRP3 inflammasome pathway, partly downregulating the inflammatory responses of M1 macrophages differentiated from THP-1 monocytes

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