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Pulmonary interstitial macrophages are required to mediate the pro-tumorigenic effects of IL-9

ABSTRACT: Pulmonary interstitial macrophages are required to mediate the pro-tumorigenic effects of IL-9

PROVIDER: PRJNA727840 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14459200_1.fastq.gz	Fastqsanger.gz
	SRR14459200_2.fastq.gz	Fastqsanger.gz
	SRR14459201_1.fastq.gz	Fastqsanger.gz
	SRR14459201_2.fastq.gz	Fastqsanger.gz
	SRR14459202_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Pulmonary interstitial macrophages are required to mediate the pro-tumorigenic effects of IL-9

Project description:We demonstrate that deficiency of IL-9 signaling inhibits lung tumor growth in multiple models. In defining the IL-9-responsive cells in the lung tumor models, we found IL-9 regulates lung heterogeneity by inhibiting alveolar macrophage and promoting the expansion of both CD11c+ and CD11c- interstitial macrophage populations. Interstitial macrophages are a critical IL-9-responsive population that is required to promote lung tumor growth. Mechanistically, the IL-9/macrophage axis requires arginase1 (Arg1) to mediate tumor growth. Adoptive transfer of Arg1+ but not Arg1- lung macrophages to Il9r-/- mice dramatically increases the tumor growth. In parallel, the elevated expression of IL-9R and Arg1 in human tumor associated macrophages is correlated with poor prognosis among lung cancer patients. Moreover, targeting IL-9 signaling in lung macrophages limited lung tumor growth.

2022-01-03 | GSE174005 | GEO

Mouse pulmonary interstitial macrophages mediate the pro-tumorigenic effects of IL-9.

Project description:Although IL-9 has potent anti-tumor activity in adoptive cell transfer therapy, some models suggest that it can promote tumor growth. Here, we show that IL-9 signaling is associated with poor outcomes in patients with various forms of lung cancer, and is required for lung tumor growth in multiple mouse models. CD4+ T cell-derived IL-9 promotes the expansion of both CD11c+ and CD11c- interstitial macrophage populations in lung tumor models. Mechanistically, the IL-9/macrophage axis requires arginase 1 (Arg1) to mediate tumor growth. Indeed, adoptive transfer of Arg1+ but not Arg1- lung macrophages to Il9r-/- mice promotes tumor growth. Moreover, targeting IL-9 signaling using macrophage-specific nanoparticles restricts lung tumor growth in mice. Lastly, elevated expression of IL-9R and Arg1 in tumor lesions is associated with poor prognosis in lung cancer patients. Thus, our study suggests the IL-9/macrophage/Arg1 axis is a potential therapeutic target for lung cancer therapy.

| S-EPMC9249769 | biostudies-literature

HDAC inhibitors promote the pro-myogenic activity of Sca1-positive interstitial cells in regenerating dystrophic muscles

Project description:We report here on the identification and functional characterization of Sca1-positive muscle interstitial cells that contribute to regeneration or fibroadipogenic degeneration of dystrophic muscles and mediate the beneficial effects of HDAC inhibitors (HDACi) in mdx mice. We found that the phenotype adopted by these cells and their biological activity are influenced by changes in muscle environment. While Sca1-positive muscle interstitial cells from healthy muscles spontaneously adopt a fibro-adipogenic phenotype, Sca1-positive muscle interstitial cells isolated from dystrophic muscles of young mdx mice show a latent myogenic phenotype that is implemented by the exposure to HDACi. Co-culture assays in vitro and co-transplantation experiments in vivo demonstrate that HDACi also improve Sca1-positive muscle interstitial cell ability to enhance the differentiation potential of adjacent satellite cells. Importantly, HDACi-induced myogenic phenotype and pro-regeneration activity were not observed in Sca1-positive muscle interstitial cells isolated from muscles of old mdx mice. The different phenotype of Sca1-positive muscle interstitial cells from mdx mice at different stages of disease progression correlated with the stage-dependent beneficial effect of HDACi, which were effective only at early stages of disease. Transplantation of Sca1-positive muscle interstitial cells isolated from regenerating young muscles into muscles of old mdx mice restored HDACi ability to increase myofiber size. These results indicate that Sca1-positive muscle interstitial cells are key cellular determinants of disease progression and mediate the beneficial effect of HDACi in a mouse model of muscular dystrophy. Isolation of Sca1+ muscle interstitial cells from TSA treated DMD/MDX mice and MuSc from DMD/MDX mice

2012-03-31 | E-GEOD-34843 | biostudies-arrayexpress

Murine Pulmonary Interstitial Macrophage Subsets after Lipopolysaccharide

Project description:Murine Pulmonary Interstitial Macrophage Subsets after Lipopolysaccharide

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Mutant p53 elicits context-dependent pro-tumorigenic phenotypes

Project description:Mutant p53 elicits context-dependent pro-tumorigenic phenotypes

| PRJNA660971 | ENA

HDAC inhibitors promote the pro-myogenic activity of Sca1-positive interstitial cells in regenerating dystrophic muscles

2012-04-01 | GSE34843 | GEO

Interstitial Macrophage Phenotypes in Schistosoma-Induced Pulmonary Hypertension

Project description:Interstitial Macrophage Phenotypes in Schistosoma-Induced Pulmonary Hypertension

| PRJNA1069761 | ENA

Mutant p53 elicits context-dependent pro-tumorigenic phenotypes (microarray)

Project description:Mutant p53 elicits context-dependent pro-tumorigenic phenotypes (microarray)

| PRJNA660982 | ENA

Characterization of murine pulmonary interstitial macrophages at steady state

Project description:In this study we demonstrate that the lung mononuclear phagocyte system comprises three interstitial macrophages (IMs), as well as alveolar macrophages (AMs), dendritic cells and few extravascular monocytes. Through cell sorting and RNAseq analysis we were able to identify transcriptional similarities and differences between the three pulmonary IM subtypes, with reference to the more well-characterized alveolar macrophage

2017-03-13 | GSE94135 | GEO

Gene expression profiling of idiopathic pulmonary fibrosis and non-specific interstitial pneumonia

Project description:Idiopathic pulmonary fibrosis (IPF) and non-specific interstitial pneumonia (NSIP) are the 2 most common forms of idiopathic interstitial pneumonia. Response to therapy and prognosis are remarkably different. The clinical-radiographic distinction between IPF and NSIP may be challenging. We sought to investigate the gene expression profile of IPF vs. NSIP We used microarray to identifiy the gene expression profiles in patients with IPF and NSIP, mixed IPF/NSIP histologic pattern and normal controls.

2018-02-06 | GSE110147 | GEO

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