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Aging imparts cell-autonomous dysfunction to regulatory T cells during recovery from influenza pneumonia

ABSTRACT: Aging imparts cell-autonomous dysfunction to regulatory T cells during recovery from influenza pneumonia

PROVIDER: PRJNA636305 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11892125.fastq.gz	Fastqsanger.gz
	SRR11892126.fastq.gz	Fastqsanger.gz
	SRR11892127.fastq.gz	Fastqsanger.gz
	SRR11892128.fastq.gz	Fastqsanger.gz
	SRR11892129.fastq.gz	Fastqsanger.gz

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Aging imparts cell-autonomous dysfunction to regulatory T cells during recovery from influenza pneumonia [RNA-seq]

Project description:Regulatory T (Treg) cells promote recovery from lung injury. Aging imparts cell-autonomous dysfunction to regulatory T cells during recovery from influenza pneumonia.

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Aging imparts cell-autonomous dysfunction to regulatory T cells during recovery from influenza pneumonia [DNA methylation/RRBS]

Project description:Regulatory T (Treg) cells promote recovery from lung injury. Aging imparts cell-autonomous dysfunction to regulatory T cells during recovery from influenza pneumonia.

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Aging imparts cell-autonomous dysfunction to regulatory T cells during recovery from influenza pneumonia [RNA-seq]

Project description:Aging imparts cell-autonomous dysfunction to regulatory T cells during recovery from influenza pneumonia [RNA-seq]

| PRJNA636352 | ENA

Aging imparts cell-autonomous dysfunction to regulatory T cells during recovery from influenza pneumonia [DNA methylation/RRBS]

Project description:Aging imparts cell-autonomous dysfunction to regulatory T cells during recovery from influenza pneumonia [DNA methylation/RRBS]

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Aging imparts cell-autonomous dysfunction to regulatory T cells during recovery from influenza pneumonia.

Project description:Regulatory T (Treg) cells orchestrate resolution and repair of acute lung inflammation and injury after viral pneumonia. Compared with younger patients, older individuals experience impaired recovery and worse clinical outcomes after severe viral infections, including influenza and SARS coronavirus 2 (SARS-CoV-2). Whether age is a key determinant of Treg cell prorepair function after lung injury remains unknown. Here, we showed that aging results in a cell-autonomous impairment of reparative Treg cell function after experimental influenza pneumonia. Transcriptional and DNA methylation profiling of sorted Treg cells provided insight into the mechanisms underlying their age-related dysfunction, with Treg cells from aged mice demonstrating both loss of reparative programs and gain of maladaptive programs. Strategies to restore youthful Treg cell functional programs could be leveraged as therapies to improve outcomes among older individuals with severe viral pneumonia.

| S-EPMC8026188 | biostudies-literature

Aging imparts cell-autonomous dysfunction to regulatory T cells during recovery from influenza pneumonia

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-02-18 | GSE151543 | GEO

Reprogrammed alveolar macrophages after pneumonia recovery

Project description:Reprogrammed alveolar macrophages after pneumonia recovery

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Impaired phagocytic function in CX3CR1+ tissue-resident skeletal muscle macrophages prevents muscle recovery after influenza A virus-induced pneumonia in aged mice

Project description:Skeletal muscle dysfunction in survivors of pneumonia is a major cause of lasting morbidity that disproportionately affects older individuals. We found that skeletal muscle recovery was impaired in aged compared with young mice after influenza A virus-induced pneumonia. In young mice, recovery of muscle loss was associated with expansion of tissue-resident skeletal muscle macrophages and downregulation of MHC II expression, followed by a proliferation of muscle satellite cells. These findings were absent in aged mice and in mice deficient in Cx3cr1. Transcriptomic profiling of tissue-resident skeletal muscle macrophages from aged compared with young mice showed downregulation of pathways associated with phagocytosis and proteostasis, and persistent upregulation of inflammatory pathways. Consistently, skeletal muscle macrophages from aged mice failed to downregulate MHCII expression during recovery from influenza A virus induced pneumonia and showed impaired phagocytic function in vitro. Like aged animals, mice deficient in the phagocytic receptor Mertk showed no macrophage expansion, MHCII downregulation or satellite cell proliferation and failed to recover skeletal muscle function after influenza A pneumonia. Our data suggest that a loss of phagocytic function in a CX3CR1+ tissue-resident skeletal muscle macrophage population in aged mice precludes satellite cell proliferation and recovery of skeletal muscle function after influenza A pneumonia.

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Project description:Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) is an emerging threat to human health throughout the world. Rodent MRSA pneumonia models mainly focus on the early innate immune responses to MRSA infection. However, the molecular pattern and mechanisms of recovery from MRSA lung infection are largely unknown. In this study, a nonlethal mouse MRSA pneumonia model was employed to investigate events during lung recovery from MRSA infection. We compared lung bacterial clearance, bronchoalveolar lavage fluid (BALF) characterization, lung histology, and gene expression profiling between Day 1 and Day 3 post-MRSA infection. Compared to Day 1 post-infection, bacterial colony counts and both BALF total cell number and protein concentration significantly decreased at Day 3 post-infection. Lung cDNA microarray analysis identified 47 significantly up-regulated and 35 down-regulated genes (p<0.01, 1.5-fold change [up and down]). Changes in eight genes were confirmed by real-time PCR. The pattern of gene expression suggests lung recovery is characterized by enhanced cell division, vascularization, and wound healing and by adjustment in host adaptive immune responses. Collectively, this data helps elucidate the molecular mechanisms of lung recovery after MRSA infection. RNA expression analysis was performed using the Illumina MouseRef-8 v2.0 BeadChip (Illumina, San Diego, CA), which provides coverage of approximately 25,700 genes and expressed sequence tags. Four independent mouse lung tissue samples at Day 1 and Day 3 post-MRSA infection were used in this study.

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