Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Macrophage peroxisomes guide alveolar regeneration and limit post-acute sequelae of SARS-CoV-2 infection (PASC)

ABSTRACT: Peroxisomes are essential but often overlooked metabolic organelles. To explore how macrophage peroxisomes protect the lung, we conducted single-cell RNA sequencing (scRNA-seq) on lungs from both naïve and SARS-CoV-2-infected Pex5^flox/flox (WT) and Cd11c-cre Pex5^flox/flox (KO) mice at 7 days post-infection (d.p.i). scRNA-seq revealed an increased proportion of inflammatory monocytes, neutrophils, and monocyte-derived macrophages (MDMs) in the lungs of infected KO mice, alongside a marked reduction in alveolar type 2 (AT2) cells and alveolar macrophages (AMs) compared to infected WT mice. AMs from KO mice showed elevated expression of genes involved in inflammatory responses, innate immunity, and cellular stress signaling, while genes related to wound healing, cell differentiation, and lipid metabolism were downregulated, compared to AMs from WT mice at 7 d.p.i.

ORGANISM(S): Mus musculus

PROVIDER: GSE280545 | GEO | 2025/03/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Macrophage peroxisomes guide alveolar regeneration and limit post-acute sequelae of SARS-CoV-2 infection (PASC).

Project description:Peroxisomes are essential but often underappreciated metabolic organelles. In this study, we demonstrate that exuberant interferon signaling reshapes the macrophage peroxisome compartment following severe COVID-19. To uncover the molecular characteristics underlying the protective role of macrophage peroxisomes after viral infection, we isolated RNA from wild-type (WT) and Pex5-deficient alveolar macrophages (AMs) with or without Poly(I:C) treatment in vitro, followed by bulk RNA sequencing. Our analysis revealed enhanced expression of inflammation-associated pathways and innate immune responses in Pex5-deficient AMs. However, these cells also exhibited attenuated activation of tissue development-related pathways and impaired mitochondrial functions, regardless of Poly(I:C) treatment.

2025-03-10 | GSE281262 | GEO

White adipose tissue from aP2-Pex5 knockout and control mice

Project description:These arrays contain data from gonodal adipose tissue of aP2-Pex5 -/- male mice 4 arrays from gonadal adipose tissue from control mice (Swiss background) are compared with 4 arrays from gonadal adipose tissue of aP2-Pex5 knockout mice. The latter lack functional peroxisomes in adipose tissue.

2012-03-01 | E-GEOD-31940 | biostudies-arrayexpress

Effect of ∆Np63 deletion on plasticity of post-injury lung basal cells

Project description:Basal cells were isolated from an influenza-infected non-tamoxifen treated Krt5CreERT2; RFP; ∆Np63flox/flox mouse and cultured, allowing for inducible ∆Np63 deletion in vitro. These basal cells were plated as monolayers, airway organoids, and alveolar organoids and treated with 1uM 4OHT for +4OHT (∆Np63 KO) or equivalent volume DMSO for -4OHT (solvent only, ∆Np63 WT). Technical triplicates of ∆Np63 WT and ∆Np63 KO were harvested for each growth condition for RNA sequencing.

2022-11-11 | GSE216160 | GEO

Bulk RNA-seq of alveolar macrophages from WT (Lepr+/+, Lyz2-Cre) and Lepr KO (Leprfl/fl, Lyz2-Cre) mice

Project description:To study the regulation of Lepr on transcriptome in WT and Lepr KO AMs under resting state and after LPS stimulation, Lepr-sufficient (Lepr+/+, Lyz2-Cre) and Lepr-deficient (Leprfl/fl, Lyz2-Cre) alveolar macrophages (AMs) were isolated by collecting BALF. Lipopolysaccharide (LPS) was added in vitro for 1h or cells were left untreated. Total RNA was extracted for deep sequencing. Gene expression in WT and Lepr KO cells were analyzed.

2022-07-20 | GSE185218 | GEO

Hypothalamus

Project description:These arrays contain data from hypthalamus tissue of nestin-Pex5 -/- male mice Gene expression in biological replicates from hypothalamus of 4 wild type mice was compared with 4 NestinPex5-/- mice. In the latter, functional peroxisomes were deleted from all neural cells.

2012-03-01 | E-GEOD-31938 | biostudies-arrayexpress

Transcriptional profiling of primary human alveolar macrophages challenged with Streptococcus pneumoniae from patients with chronic obstructive pulmonary disease compared to healthy donors

Project description:Transcriptional profiling of primary human alveolar macrophages (AMs) comparing control untreated AMs with AMs exposed with Serotype 14 Streptococcus pneumoniae (NCTC11902) strain (MOI 10) for 4 hours) Two-condition experiment, control AMs vs. infected AMs. Biological replicates: 3 control replicates, 3 infected replicates MOI 10.

2018-02-26 | E-MTAB-6491 | biostudies-arrayexpress

Transcription repressor Bach2 is required for pulmonary surfactant homeostasis and alveolar macrophage function.

Project description:Pulmonary alveolar proteinosis (PAP) results from a dysfunction of alveolar macrophages (AMs), chiefly due to disruptions in the signaling of granulocyte macrophage colony-stimulating factor (GM-CSF). We found that mice deficient for the B lymphoid transcription repressor BTB and CNC homology 2 (Bach2) developed PAP-like accumulation of surfactant proteins in the lungs. Bach2 was expressed in AMs, and Bach2-deficient AMs showed alterations in lipid handling in comparison with wild-type (WT) cells. Although Bach2-deficient AMs showed a normal expression of the genes involved in the GM-CSF signaling, they showed an altered expression of the genes involved in chemotaxis, lipid metabolism, and alternative M2 macrophage activation with increased expression of Ym1 and arginase-1, and the M2 regulator Irf4. Peritoneal Bach2-deficient macrophages showed increased Ym1 expression when stimulated with interleukin-4. More eosinophils were present in the lung and peritoneal cavity of Bach2-deficient mice compared with WT mice. The PAP-like lesions in Bach2-deficient mice were relieved by WT bone marrow transplantation even after their development, confirming the hematopoietic origin of the lesions. These results indicate that Bach2 is required for the functional maturation of AMs and pulmonary homeostasis, independently of the GM-CSF signaling. WT (n=8) and Bach2KO (n=3) AMs. One expreriment was performed.

2014-01-15 | E-GEOD-54050 | biostudies-arrayexpress

The role of Type VI collagen in alveolar bone

Project description:In this study, an α2(VI) deficient mouse (Col6α2-KO) model was used to examine the role of Type VI collagen in oral tissues. To examine bone properties, µCT was employed, and bone volume and bone mineral density (BMD) was measured in oral tissues. To further investigate its molecular basis, proteome analysis was performed using protein extracted from alveolar bone. In addition, alveolar bone loss progression was evaluated with a periodontitis induced model. µCT analysis showed the Col6α2- KO mice had less volume of alveolar bone, dentin and dental pulp, while the width of periodontal ligament (PDL) was greater than WT. The BMD in alveolar bone and dentin were elevated in Col6α2-KO mice compared with WT. Our proteome analysis showed significant changes in proteins related to ECM organization and elevation of proteins associated with biomineralization in the Col6α2-KO mice. In induced periodontitis, Col6α2-KO mice had greater alveolar bone loss compared to WT. In conclusion, Type VI collagen has role in controlling biomineralization in alveolar bone and that changes in the ECM of alveolar bone could be associated with greater bone loss from periodontitis.

2022-11-21 | PXD037422 | Pride

Bach2 keeps homeostasis in lung by regulating inflammatory response and maintaining function of alveolar macrophage.

Project description:Alveolar macrophages (AMs) of Bach2 KO mice show multiple alternations in their functions including lipid metabolism. We aimed to clarify the mechanism whereby deficiency of Bach2 impairs the function of AMs and ruins the homeostasis of lungs. Now we report that some cytokines produced from Bach2-deficient T cells alter the character of AMs and expression of Bach2 is necessary for AMs to maintain the function of lipid metabolism.

2019-02-04 | GSE79558 | GEO

Nanostring of sorted lung alveolar macrophages (AM) from cell-specific MyD88 KO at 6h after in vivo sensitization with OVA/standard flagellin

Project description:Allergic asthma is a chronic disease of the airways characterized by eosinophilic and neutrophilic inflammation. MYD88, the adaptor molecule for TLR and IL-1 family member signaling, is required for allergic sensitization through the airway in animal models of allergic asthma. We generated conditionally mutant mice separately lacking Myd88 in airway epithelial cells (ECs) or dendritic cells (DCs) and alveolar macrophages (AMs) to define the contribution of Myd88 expression in each of these cell types. To examine crosstalk from ECs to AMs in vivo, we examined transcriptional profiles from lung AMs sorted following 6h in vivo lung allergic sensitization through the airways from WT MyD88 fx/fx, SPC cre+ MyD88 fx/fx (EC-MYD88 KO), CD11c cre+ MyD88 fx/fx (DC-MYD88 KO), and full MyD88 KO mice. We observed immune-specific transcriptional changes in AMs that were cell-intrinsic as well as resulting from in vivo crosstalk from ECs. We also observed transcriptional (linked data set) and epigenetic changes in chromatin conformation in cDCs by ATAC-seq (linked data set) as well as changes in immune-specific whole lung RNA, sorted EC RNA, and sorted cDC RNA by Nanostring nCounter Immunology Codeset Analysis (additional linked files).

2018-03-10 | GSE79592 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data