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Macrophage-derived oncostatin M repairs the lung epithelial barrier during inflammatory damage

ABSTRACT: Macrophage-derived oncostatin M repairs the lung epithelial barrier during inflammatory damage

PROVIDER: PRJNA1050154 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27144229_1.fastq.gz	Fastqsanger.gz
	SRR27144229_2.fastq.gz	Fastqsanger.gz
	SRR27144230_1.fastq.gz	Fastqsanger.gz
	SRR27144230_2.fastq.gz	Fastqsanger.gz
	SRR27144231_1.fastq.gz	Fastqsanger.gz

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Macrophage-derived oncostatin M repairs the lung epithelial barrier during inflammatory damage

Project description:Macrophage-derived oncostatin M repairs the lung epithelial barrier during inflammatory damage

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Macrophage-derived oncostatin M repairs the lung epithelial barrier during inflammatory damage

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Macrophage-derived oncostatin M repairs the lung epithelial barrier during inflammatory damage

Project description:Tissue repair programs must function alongside antiviral immunity to restore the lung epithelial barrier following infection. We found that macrophage-derived oncostatin M (OSM) counteracted the pathological effects of type I interferon (IFN-I) during infection and damage in mice. At baseline, OSM-deficient mice exhibited altered alveolar type II (ATII) epithelial cell states. In response to influenza or viral mimic challenge, mice lacking OSM exhibited heightened IFN-I responses and increased mortality. Furthermore, OSM promoted organoid formation despite the growth-inhibitory effects of IFN-I. These findings identify OSM as an indispensable macrophage-derived growth factor that maintains the homeostasis of lung epithelial cells and promotes their proliferation to overcome IFN-I-mediated immunopathology.

2025-07-10 | GSE287742 | GEO

Macrophage-derived oncostatin M repairs the lung epithelial barrier during inflammatory damage

2023-12-15 | GSE249668 | GEO

Macrophage-derived oncostatin M repairs the lung epithelial barrier during inflammatory damage

Project description:Tissue repair programs must function alongside antiviral immunity to restore the lung epithelial barrier following infection. We found that macrophage-derived oncostatin M (OSM) counteracted the pathological effects of type I interferon (IFN- I) during infection and damage in mice. At baseline, OSM-deficient mice exhibited altered alveolar type II (ATII) epithelial cell states. In response to influenza or viral mimic challenge, mice lacking OSM exhibited heightened IFN-I responses and increased mortality. OSM delivery to the lung induced ATII proliferation and was sufficient to protect deficient mice against morbidity. Furthermore, OSM promoted organoid formation despite the growth- inhibitory effects of IFN- I. These findings identify OSM as an indispensable macrophage-derived growth factor that maintains the homeostasis of lung epithelial cells and promotes their proliferation to overcome IFN-I–mediated immunopathology.

2025-07-10 | GSE291698 | GEO

neonatal rat cardiomyocytes stimulated by Oncostatin M

Project description:Molecular analysis of transcriptional changes in cardiomyocytes induced by Oncostatin M treatment. The rationale of this experiment is described in [Kubin, T., et al. Oncostatin M is a major mediator of cardiomyocyte dedifferentiation and remodeling. Cell stem cell 9, 420-432 (2011)]

2015-02-27 | E-MTAB-2560 | biostudies-arrayexpress

High glucose levels increase influenza-associated damage to the pulmonary epithelial-endothelial barrier

Project description:Here, the effects of high glucose levels on influenza severity were investigated using an in vitro model of the pulmonary epithelial-endothelial barrier. We show that compared to low glucose levels, high glucose conditions prior to influenza A virus infection increased virus-induced barrier damage. Increased barrier damage was not associated with increased cell death nor increased virus replication, but rather an increased pro-inflammatory response in endothelial cells and the subsequent damage of the epithelial junctional complex.

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Gut epithelial barrier damage caused by dishwasher detergents and rinse aids

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Antibiotics damage the colonic mucus barrier in a microbiota-independent manner

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Exercise-induced Crosstalk between Immune Cells and Adipocytes in Humans: Role of Oncostatin-M

Project description:The discovery of novel exercise-regulated circulatory factors has fueled interest in the role of organ-crosstalk, especially between skeletal muscle and adipose tissue in mediating beneficial effects of exercise. We studied the adipose tissue transcriptome in men and women with normal glucose tolerance or type 2 diabetes following an acute exercise bout, revealing substantial exercise and time-dependent changes, and a sustained increase in inflammatory genes unique to Type 2 diabetes. We identify Oncostatin-M as one of the most upregulated adipose tissue secreted factors post exercise. In cultured human adipocytes, oncostatin-M enhanced MAPK signalling and regulates lipolysis. Oncostatin-M expression predominantly arises from adipose tissue immune cell fractions, while the corresponding receptors are expressed in adipocytes. Oncostatin-M expression is induced in cultured human Thp1 macrophages in response to exercise-like stimuli. Our results suggest immune cells, via secreted factors such as oncostatin-M, are important in crosstalk between skeletal muscle and adipose tissue during exercise, to regulate adipocyte metabolism and adaptation.

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