Neuroimmune connections between corticotropin-releasing hormone and mast cells: novel strategies for the treatment of neurodegenerative diseases

Bhuiyan, Piplu; Wang, Yiwei; Sha, Huanhuan; Dong, Huijuan; Qian, Yanning

doi:10.4103/1673-5374.310608

Cited by 17 publications

(10 citation statements)

References 283 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The cellular mechanism for SARS-CoV-2–inducing neuroinflammation remains unclear. Intracerebral MCs are situated close to the neurovascular region, and MC-degranulated mediators may disrupt BBB integrity, hence, promote the infiltration of inflammatory cells, and further cause brain edema and hemorrhage ( Qin et al., 2021 ; Bhuiyan et al., 2021a , Bhuiyan et al., 2021b ). In this study, we focused on investigating the role of MCs in SARS-CoV-2–induced neuroinflammation.…”

Section: Discussionmentioning

confidence: 99%

“…Intracerebral MC-degranulated mediators can increase BBB permeability by breaking down the tight junctions between brain endothelial cells, and the loss of BBB integrity may further activate meningeal MCs to recruit inflammatory cells to the CNS, leading to a vicious cycle of neuroinflammation ( Zhuang et al., 1996 ; Mattila et al., 2011 ; Vincent et al., 2016 ; Zhang et al., 2016 ). MC degranulation induced-neuroinflammation is associated with multiple neurological diseases ( Maslinska et al., 2007 ; Qin et al., 2021 ; Bhuiyan et al., 2021a , Bhuiyan et al., 2021b ).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Mast cell activation triggered by SARS-CoV-2 causes inflammation in brain microvascular endothelial cells and microglia

Wu,

Xie,

et al. 2024

Front. Cell. Infect. Microbiol.

View full text Add to dashboard Cite

SARS-CoV-2–induced excessive inflammation in brain leads to damage of blood–brain barrier, hypoxic-ischemic injury, and neuron degeneration. The production of inflammatory cytokines by brain microvascular endothelial cells and microglia is reported to be critically associated with the brain pathology of COVID-19 patients. However, the cellular mechanisms for SARS-CoV-2–inducing activation of brain cells and the subsequent neuroinflammation remain to be fully delineated. Our research, along with others’, has recently demonstrated that SARS-CoV-2–induced accumulation and activation of mast cells (MCs) in mouse lung could further induce inflammatory cytokines and consequent lung damages. Intracerebral MCs activation and their cross talk with other brain cells could induce neuroinflammation that play important roles in neurodegenerative diseases including virus-induced neuro-pathophysiology. In this study, we investigated the role of MC activation in SARS-CoV-2–induced neuroinflammation. We found that (1) SARS-CoV-2 infection triggered MC accumulation in the cerebrovascular region of mice; (2) spike/RBD (receptor-binding domain) protein–triggered MC activation induced inflammatory factors in human brain microvascular endothelial cells and microglia; (3) MC activation and degranulation destroyed the tight junction proteins in brain microvascular endothelial cells and induced the activation and proliferation of microglia. These findings reveal a cellular mechanism of SARS-CoV-2–induced neuroinflammation.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mast cell activation triggered by SARS-CoV-2 causes inflammation in brain microvascular endothelial cells and microglia

Wu,

Xie,

et al. 2024

Front. Cell. Infect. Microbiol.

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

“…Histamine, produced by mast cells, has been reported to play a role in the stress response of other species [ 6 ] as the release of corticotropin releasing hormone can induce the degranulation of mast cells under stress conditions [ 12 ]. Histamine producing bacteria have also been isolated from the rumen of cattle fed grain and the cecum of horses [ 12 ]. Although histamine can be produced and released by numerous cells within the GI tract [ 13 ] there was no increase in plasma concentrations of histamine in horses with GI disease in the present study.…”

Section: Discussionmentioning

confidence: 99%

Stress response as a contributing factor in horses with laminitis

2023

View full text Add to dashboard Cite

Background Laminitis is a complex and debilitating disease of horses. Numerous predisposing factors contribute to laminitis development, however the exact pathogenesis remains undetermined. Serum T4, cortisol, and histamine are components of the innate stress response and could play a causative or contributory role. Stress hormone concentrations in laminitis are largely unknown. Objective To evaluate parameters associated with stress response in horses with laminitis, and compare these to healthy horses and horses with gastrointestinal (GI) disease. Methods Thirty-eight adult horses presenting for non-medical conditions, GI abnormalities, or clinical laminitis were prospectively enrolled. Horses were assigned to the appropriate disease group (healthy, GI disease, and laminitis) and had blood drawn on presentation to the hospital. Samples were analyzed for plasma endogenous adrenocorticotrophic hormone (eACTH), serum cortisol, serum thyroid hormone, and plasma histamine. Results Stress hormone concentrations were significantly different between horses in the laminitis and GI disease groups. Plasma histamine levels were highest in horses with laminitis, compared with GI disease and controls. Both horses with laminitis and GI disease had increased plasma eACTH when compared to healthy horses. Horses with GI disease had higher serum cortisol concentrations than horses with laminitis or controls. Serum T4 was lower in horses with GI disease than in horses with laminitis and controls. Conclusions Horses with laminitis had relative increases in both plasma histamine and eACTH concentrations. Serum T4 and cortisol concentrations of horses with laminitis did not differ significantly when compared to healthy horses. The role of stress hormones in equine disease warrants further investigation.

show abstract

“…A studies suggested that HOXD10 [54], CCL11 [55], OLIG2 [56] and CRH (corticotropin releasing hormone) [57] can promote Alzheimer’s disease. CRH (corticotropin releasing hormone) [58] is involved in growth and development of neurodegenerative diseases. Research has shown that CRH (corticotropin releasing hormone) [59] plays an important role in the pathogenesis of hypertension.…”

Section: Discussionmentioning

confidence: 99%

Screening of the Key Genes and Signaling Pathways for Schizophrenia Using Bioinformatics and Next Generation Sequencing Data Analysis

Vastrad,

Vastrad

2023

Preprint

View full text Add to dashboard Cite

Schizophrenia is thought to be the most prevalent chronic psychiatric disorder. Numerous proteins have been identified that are associated with the occurrence and development of schizophrenia. This study aimed to identify potential core genes and pathways involved in schizophrenia, through exhaustive bioinformatic and next generation sequencing (NGS) data analyses using GSE20966 NGS data of neural progenitor cells and neurons obtained from healthy controls and patients with schizophrenia. The NGS data were downloaded from the Gene Expression Omnibus database. NGS data was processed by the DESeq2 package in R software and the differentially expressed genes (DEGs) were identified. Gene Ontology (GO) enrichment analysis and REACTOME pathway enrichment analysis were carried out to identify potential biological functions and pathways of the DEGs. Protein-protein interaction (PPI) network, module, miRNA-hub gene regulatory network and TF-hub gene regulatory network analysis were performed to identify the hub genes, miRNA and TFs. Potential hub genes were analyzed using receiver operating characteristic (ROC) curves in the R package (pROC). In this investigation, an overall 955 DEGs were identified: 478 genes were remarkably up regulated and 477 genes were distinctly down regulated. These genes were enriched for GO terms and pathways mainly involved in the multicellular organismal process, GPCR ligand binding, regulation of cellular process and amine ligand-binding receptors. MYC, FN1, CDKN2A, EEF1G, CAV1, ONECUT1, SYK, MAPK13, TFAP2A and BTK were considered the potential hub genes. miRNA-hub gene regulatory network and TF-hub gene regulatory network were constructed successfully. On the whole, the findings of this investigation enhance our understanding of the potential molecular mechanisms of schizophrenia and provide potential targets for further investigation.

show abstract

Neuroimmune connections between corticotropin-releasing hormone and mast cells: novel strategies for the treatment of neurodegenerative diseases

Cited by 17 publications

References 283 publications

Mast cell activation triggered by SARS-CoV-2 causes inflammation in brain microvascular endothelial cells and microglia

Mast cell activation triggered by SARS-CoV-2 causes inflammation in brain microvascular endothelial cells and microglia

Stress response as a contributing factor in horses with laminitis

Screening of the Key Genes and Signaling Pathways for Schizophrenia Using Bioinformatics and Next Generation Sequencing Data Analysis

Contact Info

Product

Resources

About