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Tissue damage signaling is essential for protective neutrophil recruitment to microbial infection in zebrafish (Danio rerio)

ABSTRACT: Tissue damage signaling is essential for protective neutrophil recruitment to microbial infection in zebrafish (Danio rerio)

PROVIDER: PRJNA437301 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6814870_1.fastq.gz	Fastqsanger.gz
	SRR6814870_2.fastq.gz	Fastqsanger.gz
	SRR6814880_1.fastq.gz	Fastqsanger.gz
	SRR6814880_2.fastq.gz	Fastqsanger.gz
	SRR6814890_1.fastq.gz	Fastqsanger.gz

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Integrated pathways for neutrophil recruitment and inflammation in leprosy

Project description:Neutrophil recruitment is pivotal to host defense against microbial infection, but also contributes to the immunopathology of disease. We investigated the mechanism of neutrophil recruitment in human infectious disease by bioinformatic pathways analysis of the gene expression profiles in the skin lesions of leprosy. In erythema nodosum leprosum (ENL), which occurs in patients with lepromatous leprosy (L-lep), and is characterized by neutrophil infiltration in lesions, the most overrepresented biologic functional group was “cell movement” including E-selectin, which was coordinately regulated with IL-1. In vitro activation of TLR2, upregulated in ENL lesions, triggered induction of IL-1, which together with IFN-, induced E-selectin expression on, and neutrophil adhesion to endothelial cells. Thalidomide, an effective treatment for ENL, inhibited this neutrophil recruitment pathway. The gene expression profile of ENL lesions comprised an integrated pathway of TLR2/FcR activation, neutrophil migration and inflammation, providing insight into mechanisms of neutrophil recruitment in human infectious disease. 6 ENL skin lesions and 7 Lepromatous leprosy skin lesions

2009-06-30 | E-GEOD-16844 | biostudies-arrayexpress

Integrated pathways for neutrophil recruitment and inflammation in leprosy

Project description:Neutrophil recruitment is pivotal to host defense against microbial infection, but also contributes to the immunopathology of disease. We investigated the mechanism of neutrophil recruitment in human infectious disease by bioinformatic pathways analysis of the gene expression profiles in the skin lesions of leprosy. In erythema nodosum leprosum (ENL), which occurs in patients with lepromatous leprosy (L-lep), and is characterized by neutrophil infiltration in lesions, the most overrepresented biologic functional group was 'cell movement' including E-selectin, which was coordinately regulated with IL-1beta. In vitro activation of TLR2, upregulated in ENL lesions, triggered induction of IL-1beta, which together with IFN-gamma, induced E-selectin expression on, and neutrophil adhesion to endothelial cells. Thalidomide, an effective treatment for ENL, inhibited this neutrophil recruitment pathway. The gene expression profile of ENL lesions comprised an integrated pathway of TLR2/FcR activation, neutrophil migration and inflammation, providing insight into mechanisms of neutrophil recruitment in human infectious disease.

2009-06-30 | GSE16844 | GEO

Tissue damage signaling is essential for protective neutrophil recruitment to microbial infection in zebrafish (Danio rerio)

Project description:RNAseq was performed on zebrafish larvae infected with bacteria under different osmotic pressures. The trascriptome profile generated here reveals the differential immune gene expression pattern.

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Glutamine metabolism suppresses neutrophil recruitment via epigenetic regulation to control inflammatory resolution and skin repair [Multiomic]

Project description:Tissue repair requires the resolution of inflammation. However, the molecular mechanisms that attenuate inflammation in vivo are not fully understood. Here, we identify that glutamine metabolism suppresses neutrophil recruitment to abrogate inflammation and drive tissue repair. Integrated metabolomic and transcriptional profiling identified glutamine metabolism as a key feature of macrophages during inflammatory resolution. Dietary depletion studies and conditional deletion of glutaminase (Gls), the essential enzyme involved in glutamine metabolism, in innate immune cells in mice reveals an essential role for glutamine metabolism in suppressing inflammation and promoting tissue repair. Genes involved in neutrophil recruitment are upregulated in macrophages lacking Gls and in foot ulcers of diabetic patients. Multimodal single cell transcriptomics and epigenomics reveals that Gls is required for chromatin remodeling of neutrophil recruitment genes in innate immune cells during resolution of inflammation. These findings highlight the role of glutamine metabolism in controlling cellular communication during tissue repair and suppressing neutrophil recruitment to advance inflammation resolution.

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Glutamine metabolism suppresses neutrophil recruitment via epigenetic regulation to control inflammatory resolution and skin repair [CtrlGls_RNAseq]

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Glutamine metabolism suppresses neutrophil recruitment via epigenetic regulation to control inflammatory resolution and skin repair [D1D3 RNAseq]

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Glutamine metabolism suppresses neutrophil recruitment via epigenetic regulation to control inflammatory resolution and skin repair [CUT&Tag]

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BPIFA1 Regulates Interferon-Mediated Lung Neutrophil Recruitment During Acute Inflammation

Project description:BPIFA1 Regulates Interferon-Mediated Lung Neutrophil Recruitment During Acute Inflammation

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A Liver Capsular Network of Monocyte-Derived Macrophages Restricts Hepatic Dissemination of Intraperitoneal Bacteria by Neutrophil Recruitment

Project description:Confusion arising from the attribution of divergent functions to similar cell types from the mononuclear phagocyte system is mainly due to difficulties in identifying or distinguishing different dendritic cells (DC), macrophages or monocyte subsets and/or their activation states. Using an extensive panel of surface markers and comparing in situ labelling, ex vivo flow cytometry and mass cytometry labelling together with transcriptomic analysis of sorted cells, we report the presence of a population of steady-state liver-resident macrophages populating the subcapsular space of the liver. This cell population, previously believed to be DCs, appears around weaning and is continuously replenished from adult blood-borne progenitors. Transcriptional analysis indicates that these capsule macrophages are phenotypically related to intestinal or dermis macrophages. They sensed peritoneal bacteria, promoted neutrophil recruitment to the capsule, and their specific ablation resulted in decreased neutrophil recruitment and increased intrahepatic bacterial burden. Gene expression of 2 hepatic cell subsets from 3 replicates per subset and of epidermal Langerhans cells was analyzed by microarray from purified mRNA obtained from FACS sorted CD207-GFP mice. Gene data sets were compared to those of plasmacytoid DCs (DCs), monocytes, LCs, various DCs, macrophages from the Immgen Consortium (GSE15907), dermal macrophages (GSE49358) and steady state KCs (GSE55606).

2017-08-16 | E-MTAB-5932 | biostudies-arrayexpress

Tissue Damage Signaling Is a Prerequisite for Protective Neutrophil Recruitment to Microbial Infection in Zebrafish.

Project description:Tissue damage and infection are deemed likewise triggers of innate immune responses. But whereas neutrophil responses to microbes are generally protective, neutrophil recruitment into damaged tissues without infection is deleterious. Why neutrophils respond to tissue damage and not just to microbes is unknown. Is it a flaw of the innate immune system that persists because evolution did not select against it, or does it provide a selective advantage? Here we dissect the contribution of tissue damage signaling to antimicrobial immune responses in a live vertebrate. By intravital imaging of zebrafish larvae, a powerful model for innate immunity, we show that prevention of tissue damage signaling upon microbial ear infection abrogates leukocyte chemotaxis and reduces animal survival, at least in part, through suppression of cytosolic phospholipase A2 (cPla2), which integrates tissue damage- and microbe-derived cues. Thus, microbial cues are insufficient, and damage signaling is essential for antimicrobial neutrophil responses in zebrafish.

| S-EPMC6082643 | biostudies-literature

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