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Age-associated suppression of exploratory activity during sickness is linked to meningeal lymphatic dysfunction and microglia activation [ablation]

ABSTRACT: Age-associated suppression of exploratory activity during sickness is linked to meningeal lymphatic dysfunction and microglia activation [ablation]

PROVIDER: PRJNA713919 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13944320_1.fastq.gz	Fastqsanger.gz
	SRR13944320_2.fastq.gz	Fastqsanger.gz
	SRR13944321_1.fastq.gz	Fastqsanger.gz
	SRR13944321_2.fastq.gz	Fastqsanger.gz
	SRR13944322_1.fastq.gz	Fastqsanger.gz

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Age-associated suppression of exploratory activity during sickness is linked to meningeal lymphatic dysfunction and microglia activation [ablation]

Project description:The objective of this study is to assess the contribution of meningeal lymphatic vessels to microglia response to peripheral inflammation. To this end, we sequence CD11b+ cells sorted from whole brain of adult mice with intact meningeal lymphatic vessels or mice with experimental meningeal lymphatic ablation, two hours following 1μg IL-1β or saline vehicle intraperitoneal injection. The two-hour timepoint was selected for analysis because that corresponds with the peak of the behavioral response as defined by a decrease in locomotor activity and the connection between behavior and microglia activation is of particular interest in this study.

2022-06-12 | GSE168755 | GEO

Age-associated suppression of exploratory activity during sickness is linked to meningeal lymphatic dysfunction and microglia activation [aged]

Project description:The objective of this study is to assess the contribution of meningeal lymphatic vessels to microglia response to peripheral inflammation. Aged mice (over 2 years old) were selected as a physiologically and clinically relevant model for lymphatic dysfunction because previous reporting demonstrates meningeal lymphatic function declines with age. We sequence CD11b+ cells sorted from whole brain of aged mice two hours following 1μg IL-1β or saline vehicle intraperitoneal injection. To facilitate comparison and integration with adult mouse and experimental lymphatic ablation data, identical methods were employed.

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Age-associated suppression of exploratory activity during sickness is linked to meningeal lymphatic dysfunction and microglia activation

Project description:Age-associated suppression of exploratory activity during sickness is linked to meningeal lymphatic dysfunction and microglia activation

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Age-associated suppression of exploratory activity during sickness is linked to meningeal lymphatic dysfunction and microglia activation [aged]

Project description:Age-associated suppression of exploratory activity during sickness is linked to meningeal lymphatic dysfunction and microglia activation [aged]

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CNS lymphatic drainage and neuroinflammation are regulated by meningeal lymphatic vasculature

Project description:Neuroinflammatory diseases, such as multiple sclerosis, are characterized by invasion of the brain by autoreactive T cells. The mechanism for how T cells acquire their encephalitogenic phenotype and trigger disease remains, however, unclear. The existence of lymphatic vessels in the meninges indicates a relevant link between the CNS and peripheral immune system, perhaps affecting autoimmunity. Here we demonstrate that meningeal lymphatics fulfill two critical criteria: they assist in the drainage of cerebrospinal fluid components and enable immune cells to enter draining lymph nodes in a CCR7-dependent manner. Unlike other tissues, meningeal lymphatic endothelial cells do not undergo expansion during inflammation, and they express a unique transcriptional signature. Notably, the ablation of meningeal lymphatics diminishes pathology and reduces the inflammatory response of brain-reactive T cells during an animal model of multiple sclerosis. Our findings demonstrate that meningeal lymphatics govern inflammatory processes and immune surveillance of the CNS and pose a valuable target for therapeutic intervention.

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CNS lymphatic drainage and neuroinflammation are regulated by meningeal lymphatic vasculature [2D2 T cells]

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Meningeal lymphatic dysfunction exacerbates traumatic brain injury pathogenesis

Project description:The goal of this study is to use bulk RNA-sequencing of the right brain hemisphere to observe the effects of TBI in the context of pre-existing meningeal lymphatic dysfunction in mice. We find that pre-existing meningeal lymphatic dysfunction potentiates the inflammatory response to TBI, suggesting an important role for the meningeal lymphatics in injury site drainage and proper recovery.

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Project description:The meningeal lymphatic network—housed within the dural meninges surrounding the brain— is critical for cerebrospinal fluid (CSF) drainage. Through continuous brain interstitial fluid (ISF) mixing with CSF via the glymphatic system, this lymphatic network facilitates the removal of central nervous system (CNS) waste. During aging and in Alzheimer’s disease (AD), attenuated meningeal lymphatic drainage promotes the buildup of toxic misfolded proteins—including amyloid beta—in the CNS. Alleviating this age-related meningeal lymphatic dysfunction represents a promising therapeutic strategy to alleviate AD pathology. However, the mechanisms underlying this lymphatic decline remain elusive. Here we demonstrate that age-related alterations in meningeal immunity contribute to meningeal lymphatic impairment. Single-cell RNA-sequencing of dural lymphatic endothelial cells in aged mice demonstrated a response signature to the cytokine IFNγ, which was elevated in the aged dura due to meningeal T cell accumulation. Chronic elevation of IFNγ in the meninges of young mice via AAV-mediated overexpression altered lymphatic adherans junctions and impaired CSF drainage to deep cervical lymph nodes—comparable to the deficits observed in aged mice. Direct disruption of lymphatic junctions via CSF-delivered VE-Cadherin disrupting antibodies was sufficient to phenocopy impairments in CSF drainage. Therapeutically, IFNγ neutralization in aged mice alleviated age-related impairments in meningeal lymphatic function. These data suggest manipulation of meningeal immunity as a viable therapeutic target to normalize CSF drainage in aged mice and alleviate the pathology in AD mice associated with impaired waste removal.

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