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Response of meningeal mast cells against virus infection

ABSTRACT: The role of meningeal mast cells in meningeal antiviral immunity has been poorly studied. Here we investigated the important role of meningeal mast cells in combating LCMV viral infection.

ORGANISM(S): Mus musculus

PROVIDER: GSE263668 | GEO | 2026/03/13

REPOSITORIES: GEO

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Response of meningeal stromal cells against virus infection

Project description:The role of meningeal stromal cells in meningeal antiviral immunity has been poorly studied. Here we investigated the response of meningeal stromal cells in combating LCMV viral infection.

2026-03-13 | GSE263665 | GEO

ST2 signaling orchestrates mast cell transcriptional activation during viral infection

Project description:The role of meningeal mast cells ST2 signaling in meningeal antiviral immunity has been poorly studied. Here we investigated the important role of meningeal mast cells ST2 signaling in combating LCMV viral infection.

2026-03-13 | GSE298700 | GEO

Response of meningeal mast cells against virus infection

Project description:Response of meningeal mast cells against virus infection

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Post-natal meningeal macrophages protect against viral neuroinfection

Project description:Due to the vital importance of the Central Nervous System (CNS), its potential infection and inflammation have to be tightly controlled. The surface of the CNS is connected to the periphery by a rich and complex tissue, the meninges. They contain a vast network of macrophages subdivided in at least two subpopulations endowed with elusive functions: a neonatal, MHC-II negative macrophage population, and an post-natal population expressing MHC-II. Using in situ-histocytometry, flow cytometry, and single-cell RNA sequencing approaches, we showed that those populations have opposite dynamic behaviors in response to in vivo peripheral challenges such as LPS, SARS-CoV2 and lymphocytic choriomeningitis virus (LCMV), with an apparent contraction of the MHC-II+ population. Focusing on LCMV infection in experimental mouse models and using innovative pharmacological and genetic depletion strategies, we show that meningeal macrophages (MM) represent an early line of protection against this neuroinvasive pathogen. In their absence, specific areas in the meninges became highly infected, leading to fatal brain disease. While their intrinsic sensing of viral replication through the Mitochondrial antiviral-signaling protein (MAVS) was dispensable, sensing of IFNs through the STAT1 pathway played an important role in controlling viral spread. Unexpectedly, the post-natal MHC-II+ macrophage population had an important role in controlling neuroinfection, by shutting down biosynthesis pathways and efficiently blocking viral replication. This work helps understanding the spatial organization of the brain defense system and the cellular and molecular mechanisms involved in CNS protection.

2021-12-02 | GSE189887 | GEO

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.

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Response of meningeal stromal cells against virus infection

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Gene expression profiling reveals mast cell-dependent inflammation in the meninges in early EAE.

Project description:The meninges are generally considered relatively inert tissues that house the CSF and provide protection for the brain and spinal cord. However, our previous studies using Kit mutant (Kit W/Wv) mast cell-deficient mice demonstrated that mast cells residing in the dura mater and pia mater exacerbate the severity of experimental autoimmune encephalomyelitis (EAE), the rodent model of the CNS demyelinating disease, multiple sclerosis. These data suggest that the meninges are sites of active immune responses in disease. Gene expression profiles of meningeal tissue from wild type and mast cell deficient mice prior to and at day 6 post-EAE induction were found highly distinct. Increases in both mast cell- and neutrophil-associated transcripts were among the notable disease-related changes observed in wild type mice. Kinetic analyses show that meningeal mast cells are activated within 24 hours of disease induction to express multiple mediators including IL-1b and TNF as well as the neutrophil chemoattractant, CXCL2, an observation corresponding with an influx of neutrophils to the meninges. Neutrophil recruitment as well as the disease-related loss of BBB integrity is dependent on mast cell-derived TNF. These data provide unequivocal evidence that the meninges are sites of early inflammatory events in EAE. Mast cells residing within these tissues promote disease by orchestrating an early and efficient immune cell co-localization resulting in a robust local inflammatory response and a breach of the proximal BBB. We hypothesize that these events reflect an aberrant manifestation of the normal immune surveillance role of the meninges in infection settings.

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Immunotherapy against amyloid beta is modulated by meningeal lymphatic function V

Project description:A growing body of evidence points to passive immunotherapy as a promising therapeutic strategy against AD. Herein, we show that meningeal lymphatic vasculature becomes dysfunctional in AD transgenic mice and that manipulating meningeal lymphatic drainage affects the outcome of anti-Aβ immunotherapy.

2021-03-11 | GSE160219 | GEO

Immunotherapy against amyloid beta is modulated by meningeal lymphatic function IV

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Immunotherapy against amyloid beta is modulated by meningeal lymphatic function I

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