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Effect of experimental stroke on meningeal gene expression and the influence of mast cells on these gene changes

ABSTRACT: Stroke is a leading cause of adult disability and death. Inflammation plays an important role in stroke pathology, but the factors which promote brain inflammation in this setting remain to be fully defined. Here we investigate the meninges, the membranes that envelop the brain, for a potential role in modulating immune cell trafficking to the brain. We also investigate the potential of mast cells (MCs) to modulate this response as MCs are often considered as 'first responders' playing a critical role in the initiation and development of inflammation in many disease settings. We find that stroke increases expression of inflammatory and immune response genes in the meninges in mice consistent with a potential role in modulating immune cell trafficking. Moreover, genetic and cell transfer approaches identify MCs as important modulators of this response.

ORGANISM(S): Mus musculus

PROVIDER: GSE51566 | GEO | 2014/07/31

SECONDARY ACCESSION(S): PRJNA223426

REPOSITORIES: GEO

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Effect of experimental stroke on meningeal gene expression and the influence of mast cells on these gene changes

Project description:Stroke is a leading cause of adult disability and death. Inflammation plays an important role in stroke pathology, but the factors which promote brain inflammation in this setting remain to be fully defined. Here we investigate the meninges, the membranes that envelop the brain, for a potential role in modulating immune cell trafficking to the brain. We also investigate the potential of mast cells (MCs) to modulate this response as MCs are often considered as 'first responders' playing a critical role in the initiation and development of inflammation in many disease settings. We find that stroke increases expression of inflammatory and immune response genes in the meninges in mice consistent with a potential role in modulating immune cell trafficking. Moreover, genetic and cell transfer approaches identify MCs as important modulators of this response. Three categories of male mice were used: wild-type (WT) mice, mast cell-deficient (KO) mice, and mast cell-engrafted mice (EN), which are mast cell-deficient mice repaired of their mast cell deficiency by engraftment of mast cells i.v. 8-10 weeks prior to experimentation. The mouse strain was WBB6F1-Kit+/+ (wild-type ) and WBB6F1-KitW/W-v (mast cell-deficient ). Each mouse category was subdivided into two groups, naÃ¯ve (N) and stroke (S), with n=3 per group. The stroke model was 30 minute filament occlusion of the middle cerebral artery. The dura were removed from the mouse brains at 2d post-stroke and from aged-matched naÃ¯ve mice for microarray analysis. Dura were not pooled but run on separate arrays.

2014-07-31 | E-GEOD-51566 | biostudies-arrayexpress

Stroke induces disease-specific myeloid cells in the brain parenchyma and pia

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Multi-omics and 3D-imaging reveal bone heterogeneity and unique calvaria cells in neuroinflammation

Project description:Diverse immune cells move from the calvaria marrow into the dura mater via recently discovered skull-meninges connections (SMCs). Yet, how the calvaria bone marrow is different from the other bones and whether it plays a special role in human diseases remain unknown. Using multi-omics approaches and whole mouse transparency we reveal that bone marrow cells are highly heterogeneous across the mouse body. The calvaria harbors the most distinct molecular signature with hundreds of differentially expressed genes and proteins. Acute brain injury induces skull-specific outcomes including increased calvaria cell numbers. Moreover, TSPO-PET imaging of stroke, dementia and multiple sclerosis patients demonstrate increased inflammation in the human skull, mirroring the underlying brain inflammation.

2024-01-17 | PXD030250 | Pride

Cranial photo-immunologic regulation along the skull-meninges-brain axis for promoting recovery from ischemic brain injury

Project description:Stroke involves in the interaction between central and peripheral immune systems. Skull bone marrows serve as reservoirs for immune cells in brain borders, and can rapidly respond to perturbations in the brain environment. Hence, targeting the skull bone marrow to modulate neuroimmune communications along the calvaria-meninges-brain axis would potentially improve stroke prognosis. Here, we successfully achieved cranial immunomodulation via ultraviolet (UV) irradiation of the interparietal region, which was characterized by rich marrow cavities and channels connecting the skull and meninges. Utilizing the recently-developed long-term clearing cranial window that ensured the integrity of skull, we discovered that the cranial photo-immunologic regulation (CPR) could promote cerebrovascular regeneration and aid in neurovascular repair post ischemic stroke. Single-cell transcriptome analysis revealed that meninge could be a crucial neuroimmune interface for ischemic stroke-induced immune responses. And, CPR could restore the stroke-induced alterations in cellular gene expression, especially meningeal B cells. Further we demonstrated that CPR could effectively alleviate the excessive suppression of meningeal B cell activation caused by ischemic stroke. This work opens avenues for immunoregulation through the skull-meninges-brain axis and provides valuable insights for immunomodulatory therapies in brain diseases.

2024-04-18 | GSE254550 | GEO

Cranial photo-immunologic regulation along the skull-meninges-brain axis for promoting recovery from ischemic brain injury

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Transfer RNA fragments replace microRNA regulators of the cholinergic post-stroke immune blockade III

Project description:After ischemic stroke, the brain initiates intensive communication with the immune system, and acetylcholine contributes to this process. Stroke triggers peripheral immunosuppression leading to increased susceptibility to infections; and post-stroke pneumonia is linked with poor stroke outcome, but the responsible processes are yet unknown. We discovered a “change of guards” where microRNA levels decreased but small transfer RNA fragments (tRFs) accumulated in post-stroke blood cells. This molecular switch may re-balance acetylcholine signaling in CD14+ monocytes by regulating their gene expression and modulating post-stroke immunity. Our observations point to tRFs as new molecular regulators of post-stroke immune responses that may become potential therapeutic targets.

2020-12-31 | GSE158313 | GEO

Transfer RNA fragments replace microRNA regulators of the cholinergic post-stroke immune blockade II

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Transfer RNA fragments replace microRNA regulators of the cholinergic post-stroke immune blockade I

2020-12-31 | GSE158311 | GEO

Protective monocytes in cerebral ischemia

Project description:Stroke is a highly prevalent and devastating disease with limited therapeutic options. Most efforts to develop treatments for stroke have thus far met with limited success in large clinical trials. The brain has an enormous capacity for self-preservation, and elucidating how the brain protects itself may provide novel insights into stroke treatment. Ischemic tolerance (IT), a phenomenon in which application of sub-lethal stress [preconditioning (PC) stimulus; PC] induces a state of tolerance to a subsequent ischemic insult, represents an example of endogenous neuroprotection. IT can be induced in brain by systemic administration of the Toll-like receptor-4 ligand lipopolysaccharide (LPS). Different populations of immune cell could potentially play a role in PC induced by LPS. In particular, monocytes, which are the main target of LPS, can exert a powerful protective effect either directly or by modulating the immune system.

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Project description:The meninges are densely innervated by nociceptive sensory neurons that mediate pain and headache. How pain and neuro-immune interactions impact meningeal host defenses is unclear. Bacterial meningitis causes life-threatening infections of the meninges and central nervous system (CNS), affecting over one million people a year. Here we find that Nav1.8+ neuron signaling to immune cells in the meninges via the neuropeptide calcitonin gene-related peptide (CGRP) exacerbates bacterial meningitis. Nociceptor ablation reduced meningeal and brain invasion by two bacterial pathogens: Streptococcus pneumoniae and Streptococcus agalactiae. S. pneumoniae activated nociceptors via Pneumolysin to release CGRP, which acts through its receptor RAMP1 on meningeal macrophages to inhibit chemokine expression, neutrophil recruitment and antimicrobial defenses. Macrophage-specific RAMP1 deficiency or blockade of RAMP1 signaling enhanced immune responses and bacterial clearance in meninges and brain. Therefore, targeting a neuro-immune axis in the meninges can enhance host defenses and may be a potential treatment for bacterial meningitis.

2022-12-23 | GSE221681 | GEO

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