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

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

PROVIDER: PRJNA636351 | ENA |

REPOSITORIES: ENA

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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.

2021-02-18 | GSE151541 | GEO

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.

2021-02-18 | GSE151542 | GEO

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

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

| PRJNA636305 | ENA

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.

Project description: Not available

| 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:Community-acquired pneumonia is a widespread disease with significant morbidity and mortality. Alveolar macrophages are tissue-resident lung cells that play a crucial role in innate immunity against bacteria causing pneumonia. We hypothesized that alveolar macrophages display adaptive characteristics after resolution of bacterial pneumonia. We studied mice one to six months after self-limiting lung infection due to Streptococcus pneumoniae, the most common cause of bacterial pneumonia. Among the myeloid cells recovered from the lung, only alveolar macrophages showed long-term modifications of their surface marker phenotype. The remodeling of alveolar macrophages was: (i) long-lasting (still observed 6 months post infection), (ii) regionally localized (only observed in the affected lobe after lobar pneumonia), and (iii) associated with a macrophage-dependent enhanced lung protection to another pneumococcal serotype. Metabolomic and transcriptomic profiling revealed that alveolar macrophages of mice which recovered from pneumonia had new baseline activities and altered responses to infection. Thus, the enhanced lung protection after mild and self-limiting respiratory infection includes a profound remodeling of alveolar macrophages that is long-lasting, compartmentalized, and manifest across surface receptors, metabolites, and both resting and stimulated transcriptomes. We used microarrays to detail the global program of gene expression for mouse alveolar macrophages sorted from lungs that were naïve or infected more than a month previously, at rest and during an acute (4-hour) infection.

2020-04-17 | GSE133975 | GEO

Reprogrammed alveolar macrophages after pneumonia recovery

Project description:Reprogrammed alveolar macrophages after pneumonia recovery

| PRJNA553227 | ENA

Mouse livers during pneumonia

Project description:This SuperSeries is composed of the following subset Series: GSE32105: Expression data from mouse livers lacking STAT3 and RelA during pneumonia GSE35513: Expression data from mouse livers lacking NF-kappaB RelA (p65) during pneumonia GSE35514: Expression data from mouse livers lacking STAT3 during pneumonia GSE35515: Expression data from mouse livers expressing or lacking Cre recombinase during pneumonia Refer to individual Series

2012-02-16 | E-GEOD-35516 | biostudies-arrayexpress

Transcriptional events during lung recovery from MRSA infection: a mouse pneumonia model

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.

2013-11-12 | E-GEOD-36587 | biostudies-arrayexpress

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