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GM-CSF controls Mycobacterium tuberculosis infection by limiting type I IFN-driven neutrophil extracellular trap formation [Lung]

ABSTRACT: GM-CSF controls Mycobacterium tuberculosis infection by limiting type I IFN-driven neutrophil extracellular trap formation [Lung]

PROVIDER: PRJNA592572 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10560700_1.fastq.gz	Fastqsanger.gz
	SRR10560700_2.fastq.gz	Fastqsanger.gz
	SRR10560701_1.fastq.gz	Fastqsanger.gz
	SRR10560701_2.fastq.gz	Fastqsanger.gz
	SRR10560702_1.fastq.gz	Fastqsanger.gz

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GM-CSF controls Mycobacterium tuberculosis infection by limiting type I IFN-driven neutrophil extracellular trap formation

Project description:GM-CSF controls Mycobacterium tuberculosis infection by limiting type I IFN-driven neutrophil extracellular trap formation

| PRJNA592569 | ENA

GM-CSF controls Mycobacterium tuberculosis infection by limiting type I IFN-driven neutrophil extracellular trap formation [Lung]

Project description:Tuberculosis (TB) remains the world’s top infectious killer. Understanding how immune mediators determine the outcome of Mycobacterium tuberculosis infection could facilitate the design of better therapies against this devastating disease. GM-CSF mediates protective immunity against TB but the underlying mechanisms remain elusive. To determine the molecular mechanisms underlying the protective role of GM-CSF during M. tuberculosis infection we performed RNA-sequencing analyses of whole blood and lung samples obtained from C57Bl/6 mice infected with HN878 and treated with anti-GM-CSF monoclonal antibody or isotype control. Uninfected mice were also treated and used as uninfected controls. Three weeks post-infection, whole blood and lungs were harvested from each individual mouse and processed for RNA-sequencing. Transcriptomic analyses revealed that during M. tuberculosis infection GM-CSF regulates the expression of genes associated with neutrophil recruitment and activation and type I IFN-inducible genes, which have been previously associated with TB pathogenesis. Further mechanistical studies showed that disease exacerbation driven by GM-CSF blockade during M. tuberculosis infection was type I IFN and neutrophil-dependent and that over-activation of neutrophils by type I IFN induced NET formation at the site of infection. NETs were also found in necrotic lung lesions from patients with pulmonary TB and type I IFN-driven NET formation correlated with increased disease susceptibility in different mouse models of TB. Our findings reveal an important immune network that may play a central role in determining TB outcome.

2020-09-07 | GSE141205 | GEO

GM-CSF controls Mycobacterium tuberculosis infection by limiting type I IFN-driven neutrophil extracellular trap formation [Blood]

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GM-CSF controls Mycobacterium tuberculosis infection by limiting type I IFN-driven neutrophil extracellular trap formation [Blood]

Project description:GM-CSF controls Mycobacterium tuberculosis infection by limiting type I IFN-driven neutrophil extracellular trap formation [Blood]

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NKp46+ ILC3s promote early neutrophil defense against C. difficile infection through GM-CSF secretion

Project description:Clostridioides difficile infection (CDI) is a common cause of antibiotic-associated colitis. C. difficile proliferates and produces toxins that damage the colonic epithelium, leading to symptoms ranging from mild diarrhea to severe pseudomembranous colitis. The host's innate response to CDI occurs in two phases: an early phase in which neutrophils reduce the bacterial load, and a late phase involving repair mechanisms to restore epithelial integrity. Group 3 innate lymphoid cells (ILC3s) are crucial in protecting the gut from CDI. Previous studies have shown that ILC3 production of IL-22 is essential in the late phase of CDI for epithelial repair and maintaining an intestinal microbiota that competes with C. difficile, preventing its expansion. Our study finds that ILC3s also protect during the early stages of CDI by sustaining neutrophils through GM-CSF. Less neutrophil production, accumulation and activation was evident in ILC3-deficient mice than in wild-type (WT) mice, which led to exacerbated symptoms, impaired pathogen clearance, a compromised epithelial barrier, and increased mortality. The adoptive transfer of ILC3s into ILC3-deficient mice restored neutrophil responses and improved disease outcomes. Both in vitro and in vivo experiments revealed that GM-CSF production by ILC3s is crucial for neutrophil production and effective resistance during CDI. Using mice lacking NKp46+ ILC3s, we found that this subset significantly contributes to GM-CSF production in CDI. These findings highlight the critical role of the ILC3-neutrophil connection in early innate responses to CDI. Enhancing ILC3 production of GM-CSF could be a promising strategy for improving host defense against CDI and other enteric infections.

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miRNA expression microarrays in GM-CSF or GM-CSF+IL6-induced mouse MDSC

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2017-10-09 | GSE104719 | GEO

NK cell-derived GM-CSF potentiates autoantibody-induced inflammatory arthritis and is negatively regulated by CIS

Project description:To examine the effect of CIS-deficiency on neutrophil inflammation-associated transcriptional profile in response to GM-CSF signalling

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mRNA and long noncoding RNA expression microarrays in GM-CSF or GM-CSF+IL6-induced mouse MDSC

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Proteomic analysis of GM-CSF and M-CSF polarized bone marrow derived macrophages

Project description:Bone marrow cells were isolated, primed with M-CSF (M-BMDM) or GM-CSF (GM-BMDM) and cultured for 7 days. The proteomic difference between GM-BMDM and M-BMDM were analyzed to describe the phenotye and function of two types of macrophages.

2023-03-29 | PXD041180 |

GM-CSF induced gene-regulation in human monocytes

Project description:Human and murine studies showed that granulocyte macrophage colony-stimulating factor (GM-CSF) exerts beneficial effects in intestinal inflammation. To explore whether GM-CSF mediates its effects via monocytes, we analyzed effects of GM-CSF on monocytes in vitro and assessed the immunomodulatory potential of GM-CSF-activated monocytes (GMaM). We used microarray technology and functional assays to characterize GMaM in vitro and used a mouse model of colitis to study GMaM functions in vivo.

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