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Ketogenesis restrains aging-induced exacerbation of COVID in a mouse model (scRNA-seq)

ABSTRACT: Ketogenesis restrains aging-induced exacerbation of COVID in a mouse model (scRNA-seq)

PROVIDER: PRJNA649448 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12343753.fastq.gz	Fastqsanger.gz
	SRR12343754.fastq.gz	Fastqsanger.gz
	SRR12343755.fastq.gz	Fastqsanger.gz
	SRR12343756.fastq.gz	Fastqsanger.gz

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Ketogenesis restrains aging-induced exacerbation of COVID in a mouse model

Project description:Ketogenesis restrains aging-induced exacerbation of COVID in a mouse model

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Ketogenesis restrains aging-induced exacerbation of COVID in a mouse model (bulk RNA-seq)

Project description:Ketogenesis restrains aging-induced exacerbation of COVID in a mouse model (bulk RNA-seq)

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Ketogenesis restrains aging-induced exacerbation of COVID in a mouse model (scRNA-seq)

Project description:Impaired immunometabolic response in the elderly regulates inflammation-driven COVID-19 severity which confers the greatest risk of mortality. To investigate how aging compromises defense against COVID-19, we developed a model of natural murine beta coronavirus (mCoV) infection with mouse hepatitis virus strain A59 (mCoV-A59) that recapitulated majority of hallmarks of COVID-19. Aged mCoV-A59-infected mice have increased mortality and higher systemic inflammation in the heart, adipose tissue and hypothalamus, including neutrophilia and loss of γδ T cells in lungs. Ketogenic diet increases beta-hydroxybutyrate, expands tissue protective γδ T cells, deactivates the inflammasome and decreases pathogenic monocytes in lungs during aging. These data underscore the value of mCoV-A59 model to test mechanism and establishes harnessing of ketogenic immunometabolic checkpoint as potential treatment against COVID-19 in the elderly.

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Ketogenesis restrains aging-induced exacerbation of COVID in a mouse model

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Project description:As coronavirus disease 2019 (COVID-19) and aging are both accompanied by cognitive decline, we hypothesized that COVID-19 might lead to molecular signatures similar to aging. We performed whole-transcriptome analysis of the frontal cortex, a critical area for cognitive function, in individuals with COVID-19, age-matched and sex-matched uninfected controls, and uninfected individuals with intensive care unit/ventilator treatment. Our findings indicate that COVID-19 is associated with molecular signatures of brain aging and emphasize the value of neurological follow-up in recovered individuals.

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Project description:Aging is identified as a significant risk factor for severe coronavirus disease-2019 (COVID-19), often resulting in profound lung damage and mortality. Yet, the biological relationship between aging, aging-related comorbidities, and COVID-19 remains incompletely understood. This study aimed to elucidate the age-related COVID19 pathogenesis using a Hutchinson-Gilford progeria syndrome (HGPS) mouse model with humanized ACE2 receptors. Pathological features were compared between young, aged, and HGPS hACE2 mice following SAR-CoV-2 challenge. We demonstrated that young mice display robust interferon response and antiviral activity, whereas this response is attenuated in aged mice. Viral infection in aged mice results in severe respiratory tract bleeding, likely contributing a higher mortality rate. In contrast, HGPS hACE2 mice exhibit milder disease manifestations characterized by minor immune cell infiltration and dysregulation of multiple metabolic processes. Comprehensive transcriptome analysis revealed both shared and unique gene expression dynamics among different mouse groups. Collectively, our studies evaluated the impact of SARS-CoV-2 infection on progeroid syndromes using a HGPS hACE2 mouse model, which holds promise as a valuable tool for investigating COVID-19 pathogenesis in individuals with premature aging.

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Ketogenic diet restrains aging-induced exacerbation of coronavirus infection in mice.

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