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Neutrophil extracellular traps activate IL-8 and IL-1 expression in human bronchial epithelia

ABSTRACT: Neutrophil extracellular traps activate IL-8 and IL-1 expression in human bronchial epithelia

PROVIDER: PRJNA511873 | ENA |

REPOSITORIES: ENA

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Neutrophil extracellular traps activate IL-8 and IL-1 expression in human bronchial epithelia

Project description:Human Broncial Epithilal cells (HBEs) exposed to NETs compared to HBEs exposed to PBS show upregulatation of genes, most of which were related to IL-1 family members and GM-CSF.

2020-04-01 | GSE124378 | GEO

Neutrophil extracellular traps activate IL-8 and IL-1 expression in human bronchial epithelia.

Project description:Neutrophil extracellular traps (NETs) provide host defense but can contribute to the pathobiology of diverse human diseases. We sought to determine the extent and mechanism by which NETs contribute to human airway cell inflammation. Primary normal human bronchial epithelial cells (HBEs) grown at air-liquid interface and wild-type (wt)CFBE41o- cells (expressing wtCFTR) were exposed to cell-free NETs from unrelated healthy volunteers for 18 h in vitro. Cytokines were measured in the apical supernatant by Luminex, and the effect on the HBE transcriptome was assessed by RNA sequencing. NETs consistently stimulated IL-8, TNF-α, and IL-1α secretion by HBEs from multiple donors, with variable effects on other cytokines (IL-6, G-CSF, and GM-CSF). Expression of HBE RNAs encoding IL-1 family cytokines, particularly IL-36 subfamily members, was increased in response to NETs. NET exposure in the presence of anakinra [recombinant human IL-1 receptor antagonist (rhIL-1RA)] dampened NET-induced changes in IL-8 and TNF-α proteins as well as IL-36α RNA. rhIL-36RA limited the increase in expression of proinflammatory cytokine RNAs in HBEs exposed to NETs. NETs selectively upregulate an IL-1 family cytokine response in HBEs, which enhances IL-8 production and is limited by rhIL-1RA. The present findings describe a unique mechanism by which NETs may contribute to inflammation in human lung disease in vivo. NET-driven IL-1 signaling may represent a novel target for modulating inflammation in diseases characterized by a substantial NET burden.

| S-EPMC7468846 | biostudies-literature

Specific post-translational histone mod. of neutrophil extracellular traps as immunogens & potential SLE Ab targets.

Project description:This SuperSeries is composed of the following subset Series: GSE32542: Murine serum reactivity to common autoantigens in response to immunization with neutrophil extracellular traps GSE32543: Human and murine serum reactivity to specific histone posttranslational modifications in neutrophil extracellular traps Refer to individual Series

2012-01-26 | E-GEOD-32544 | biostudies-arrayexpress

The cytosolic DNA sensor cGAS recognizes Neutrophil Extracellular Traps

Project description:Neutrophil Extracellular Traps (NETs) are structures consisting of chromatin and antimicrobial molecules that are released by neutrophils during a form of regulated cell death called NETosis. NETs trap invading pathogens, promote coagulation and activate myeloid cells to produce Type I interferons (type I IFN), proinflammatory cytokines that regulate the immune system. The mechanism of NET recognition by myeloid cells is not yet clearly identified. Here we show that macrophages and other myeloid cells phagocytose NETs. Once in phagosomes, NETs translocate to the cytosol, where they activate the DNA sensor cyclic GMP-AMP synthase (cGAS) and induce type I IFN expression. cGAS recognizes the DNA backbone of NETs. Interestingly, the NET associated serine protease Neutrophil Elastase (NE) mediates the activation of the pathway. We confirmed that NETs activate cGAS in vivo. Thus, our findings identify cGAS as a major sensor of NETs, mediating the immune activation during infection and in auto-immune diseases.

2021-02-18 | PXD015579 | Pride

Piezo1 induces neutrophil extracellular traps formation directing M1 macrophage differentiation

Project description:To research the neutrophil extracellular traps in the regulation of macrophages differentiation, we performed gene expression profiling analysis using data obtained from RNA-seq of mice and control with virus infection.

2024-07-10 | GSE220198 | GEO

RNA sequencing of healthy human airway epithelia with IL-13 treatment time course

Project description:The goal of this study was to examine changes to gene expression induced by IL-13 treatment of air-liquid interface cultures of healthy primary human airway epithelia over time.

2023-08-16 | GSE240741 | GEO

Inflammation and neutrophil extracellular traps in cerebral cavernous malformation

Project description:Cerebral Cavernous Malformation (CCM) is a brain vascular disease with various neurological symptoms. In this study, we describe the inflammatory profile in CCM and show for the first time the formation of neutrophil extracellular traps (NETs) in rodents and humans with CCM. Through RNA-seq analysis of cerebellum endothelial cells from wild-type mice and mice with anendothelial cell-specific ablation of the Ccm3 gene (Ccm3iECKO), we show that endothelial cells from Ccm3iECKO mice have anincreased expression of inflammation-related genes.

2023-10-31 | GSE246373 | GEO

Neutrophil Extracellular Traps Activate Proinflammatory Functions of Human Neutrophils.

Project description:Neutrophil extracellular traps (NETs) consist of decondensed nuclear chromatin that is associated with proteins and are released by neutrophils during an inflammatory response. Released NETs are able to capture pathogens, prevent their dissemination and potentially kill them via antimicrobial peptides and proteins that are associated with the decondensed chromatin. In addition to their antimicrobial functions, NETs have also been shown to exert immunomodulatory effects by activation and differentiation of macrophages, dendritic cells and T cells. However, the effect of NETs on neutrophil functions is poorly understood. Here we report the first comprehensive study regarding the effects of NETs on human primary neutrophils in vitro. NETs were isolated from cultures of PMA-exposed neutrophils. Exposure of neutrophils to isolated NETs resulted in the activation of several neutrophil functions in a concentration-dependent manner. NETs induced exocytosis of granules, the production of reactive oxygen species (ROS) by the NADPH oxidase NOX2, NOX2-dependent NET formation, increased the phagocytosis and killing of microbial pathogens. Furthermore, NETs induced the secretion of the proinflammatory chemokine IL-8 and the B-cell-activating cytokine BAFF. We could show that the NET-induced activation of neutrophils occurs by pathways that involve the phosphorylation of Akt, ERK1/2 and p38. Taken together our results provide further insights into the proinflammatory role of NETs by activating neutrophil effector function and further supports the view that NETs can amplify inflammatory events. On the one hand the amplified functions enhance the antimicrobial defense. On the other hand, NET-amplified neutrophil functions can be involved in the pathophysiology of NET-associated diseases. In addition, NETs can connect the innate and adaptive immune system by inducing the secretion of the B-cell-activating cytokine BAFF.

| S-EPMC8217666 | biostudies-literature

mRNA, ncRNA-seq and miRNA-seq of AGS cellline and AGS cellline with neutrophil extracellular traps

Project description:ncRNA-seq and miRNA-seq of AGS cellline and AGS cellline with neutrophil extracellular traps

2022-05-18 | GSE188741 | GEO

Single cell RNA sequencing of healthy human airway epithelia with IL-13 treatment time course

Project description:The goal of this study was to examine changes in cell composition and gene expression with IL-13 treatment over time within different cell types from air-liquid interface cultures from healthy primary human airway epithelia.

2024-04-12 | GSE229202 | GEO

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