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Characterization of cell subsets in lung tissue from mice treated with or without MSDC-0602K following influenza virus infection

ABSTRACT: To understand how a new insulin sensitizer MSDC-0602K affects lung phenotype in vivo, lungs from WT mice treated with DMSO or a new insulin sensitizer MSDC-0602K at day 4 post influenza virus infection were utilized for single-cell RNA sequencing analysis. Dimensionality reduction analysis of combined DMSO or MSDC-0602K-treated lungs revealed 25 clusters based on their gene expression pattern, and cells from those two groups showed similarity as visualized in UMAP plot. Interestingly, MSDC-0602K treatment diminished infiltration of proinflammatory cell types including monocytes or neutrophils while increased percentage of alveolar macrophages or Type I epithelial cells compared to DMSO treatment. Moreover, a number of proinflammatory gene expression was decreased in alveolar macrophages in lungs from MSDC-0602K treated mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE181798 | GEO | 2023/02/23

REPOSITORIES: GEO

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Transcriptomic analysis of lung tissue from WT mice treated with or without MSDC-0602K following influenza virus infection

Project description:To identify molecular characteristics of lung tissue from WT mice treated with DMSO or a new insulin sensitizer MSDC-0602K at day 4 post influenza virus infection, we isolated RNA from lungs with various treatments and examined by bulk RNA-seq. We found a large number of gene profiles were altered following MSDC-0602K treatment in lungs. Interestingly, gene sets involved inflammatory responses were enriched in DMSO treatd mouse lungs whereas gene set of fatty acid metabolism was enriched in MSDC-0602K treated mouse lung, suggesting MSDC-0602K treatment diminshed pulmonary inflammation and altered metabolic status during influenza virus infection.

2023-02-23 | GSE181776 | GEO

Transcriptomic analysis of lung tissue from db/db mice treated with or without MSDC-0602K following influenza virus infection

Project description:To identify molecular characteristics of lung tissue from db/db mice treated with DMSO or a new insulin sensitizer MSDC-0602K at day 5 post influenza virus infection, we isolated RNA from lungs with various treatments and examined by bulk RNA-seq. We found a large number of gene profiles were altered following MSDC-0602K treatment in lungs. Interestingly, a number of genes accounting for pulmonary inflammatory responses were significantly decreased following MSDC-0602K treatment in lungs of db/db mice at day 5 post influenza virus infection. Moreover, MSDC-0602K treated lung tissue showed lower levels of genes related to glucose metabolism.

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Mus musculus

Project description:PPARg controls proinflammatory responses in alveolar macrophages

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Capacity of yolk sac macrophages, fetal liver and adult monocytes to colonize an empty niche and develop into functional tissue resident macrophages

Project description:Tissue-resident macrophages can derive from yolk sac macrophages, fetal liver monocytes or adult bone marrow monocytes. Whether these precursors can give rise to transcriptionally identical alveolar macrophages is unknown. Here, we transferred traceable yolk sac macrophages, fetal liver monocytes, adult bone marrow monocytes or adult alveolar macrophages as a control, into the empty alveolar macrophage niche of neonatal Csf2rb-/- mice. All precursors efficiently colonized the alveolar niche and generated alveolar macrophages that were transcriptionally almost identical, with only 22 genes that could be linked to their origin. Underlining the physiological relevance of our findings, all transfer-derived alveolar macrophages self-maintained within the lungs for up to 1 year and durably prevented alveolar proteinosis. Thus, precursor origin does not affect the development of functional self-maintaining tissue-resident macrophages. CD45.1+CD45.2+ yolk sac macrophages, fetal liver monocytes, adult bone marrow monocytes or adult alveolar macrophages from the bronchoalveolar lavage were sorted from wild type CD45.1+CD45.2+ mice of indicated ages. From part of these samples RNA was isolated. The other part was transferred intranasally into the lungs of neonate Csf2rb-/- mice. 6 weeks post-transfer, transfer-derived CD45.1+CD45.2+ alveolar macrophages were sorted from the bronchoalveolar lavage. Wild type CD45.1+CD45.2 alveolar macrophages from the bronchoalveolar lavage of 6 week old mice were sorted as control. 36 samples (arrays) in total. RNA was isolated, amplified with Nugene pico kit, converted to cDNA and then hybridised on Affymetrix GeneChip Mouse Gene 1.0 ST Arrays.

2016-03-01 | E-GEOD-76999 | biostudies-arrayexpress

Capacity of yolk sac macrophages, fetal liver and adult monocytes to colonize an empty niche and develop into functional tissue resident macrophages

2016-03-01 | GSE76999 | GEO

Genome-wide analysis of whole-lung and alveolar macrophages before and after gut microbiome depletion

Project description:Pneumonia accounts for more deaths than any other infectious disease worldwide. The intestinal microbiota has emerged as a key defense system by local support of mucosal immunity as well as proposed modulatory effects on systemic immunity. We here investigated the transcriptomes of whole-lungs and alveolar macrophages between untreated and antibiotic treated mice.

2016-12-09 | GSE53174 | GEO

Expression data from E18.5 Igf1 -/- (homozygous mutant) and Igf1+/+ (normal wild type control) mouse lungs

Project description:Insight into the role of Insulin-like Growth Factor (IGF) in development of lungs has come from the study of genetically modified mice. IGF1 is a key factor during lung development. IGF1 deficiency in the neonatal mouse causes respiratory failure collapsed alveoli and altered alveolar septa. To further characterize IGF1 function during lung development we analyzed Igf1-/- mouse prenatal lungs in a C57Bl/6 genetic background. Mutant lungs showed disproportional hypoplasia, disorganized extracellular matrix and dilated alveolar capillaries. IGF1 target genes during lung maturation were identified by analyzing RNA differential expression in Igf1-/- lungs using microarrays.

2014-03-31 | GSE17157 | GEO

Ontogeny of alveolar macrophages is a critical determinant of function during lung fibrosis [RNA-seq]

Project description:Little is known about the relative importance of monocyte and tissue-resident macrophages in the development of lung fibrosis. We show that specific genetic deletion of monocyte-derived alveolar macrophages after their recruitment to the lung ameliorated lung fibrosis, whereas tissue-resident alveolar macrophages did not contribute to fibrosis. Using transcriptomic profiling of flow-sorted cells, we found that monocyte to alveolar macrophage differentiation unfolds continuously over the course of fibrosis and its resolution. During the fibrotic phase, monocyte-derived alveolar macrophages differ significantly from tissue-resident alveolar macrophages in their expression of profibrotic genes. A population of monocyte-derived alveolar macrophages persisted in the lung for one year after the resolution of fibrosis, where they became increasingly similar to tissue-resident alveolar macrophages. Human homologues of profibrotic genes expressed by mouse monocyte-derived alveolar macrophages during fibrosis were up-regulated in human alveolar macrophages from fibrotic compared with normal lungs. Our findings suggest that selectively targeting alveolar macrophage differentiation within the lung may ameliorate fibrosis without the adverse consequences associated with global monocyte or tissue-resident alveolar macrophage depletion.

2017-06-25 | GSE82158 | GEO

Expression data from E18.5 Igf1 -/- (homozygous mutant) and Igf1+/+ (normal wild type control) mouse lungs

2014-03-31 | E-GEOD-17157 | biostudies-arrayexpress

Tartrate resistant acid phosphatase 5 (TRAP5) mediates immune cell recruitment in a murine model of pulmonary bacterial infection

Project description:During airway infection, upregulation of proinflammatory cytokines and subsequent immune cell recruitment is essential to mitigate bacterial infection. Conversely, during prolonged and non-resolving airway inflammation, neutrophils contribute to tissue damage and remodeling. This occurs during diseases including cystic fibrosis (CF) and COPD where bacterial pathogens, not least Pseudomonas aeruginosa, contribute to disease progression through long-lasting infections. Tartrate-resistant acid phosphatase (TRAP) 5 is a metalloenzyme expressed by alveolar macrophages and one of its target substrates is the phosphoglycoprotein osteopontin (OPN). In this study, we found that TRAP5-/- mice had impaired clearance of P. aeruginosa airway infection and reduced recruitment of immune cells. TRAP5 knockdown using siRNA resulted in a decreased activation of the proinflammatory transcription factor NF‐B in reporter mice and a subsequent decrease of proinflammatory gene expression. Add‐back experiments of enzymatically active TRAP5 to TRAP5-/- mice restored immune cell recruitment and bacterial killing. In human CF lung tissue, TRAP5 of alveolar macrophages was detected in proximity to OPN to a higher degree than in normal lung tissue, indicating possible interactions. Taken together, the findings of this study suggest a key role for TRAP5 in modulating airway inflammation. This could have bearing in diseases such as CF and COPD where excessive sterile inflammation could be targeted by pharmacological inhibitors of TRAP5.

2022-12-30 | PXD038135 | Pride

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