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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.

2018-05-15 | GSE111528 | GEO

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.

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Project description:Macrophage-Endothelial Cell Crosstalk Orchestrates Neutrophil Recruitment in Inflamed Mucosa scRNA-Seq

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Macrophage-Endothelial Cell Crosstalk Orchestrates Neutrophil Recruitment in Inflamed Mucosa RNA-Seq

Project description:Macrophage-Endothelial Cell Crosstalk Orchestrates Neutrophil Recruitment in Inflamed Mucosa RNA-Seq

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IL-17 activates dermal reticular fibroblasts to promote neutrophil recruitment and host defense [scRNAseq]

Project description:The complex system by which the skin regulates immune responses to the external environment is unclear. Here, we investigated cell-cell interactions underlying cutaneous defense against S. aureus. Single-cell transcriptomics (scRNA-Seq) and unbiased network analysis revealed unexpected, dominant IL-17-mediated dermal reticular fibroblast-to-neutrophil communication. Multi-faceted in vitro omics studies demonstrated that IL-17 synergized with several factors including TNF⍺ to induce fibroblast NFKBIZ and chemokine secretion. Cultured fibroblasts drove robust neutrophil recruitment through NFKBIZ-dependent CXCR2 and CXCR4 ligands. Mice lacking IL-17R in fibroblasts (PdgfraΔIl17ra) were generated to determine the significance of fibroblast-neutrophil communication. PdgfraΔIl17ra mice exhibited drastically reduced skin neutrophilia in multiple disease models and reduced defense against S. aureus. These findings were translated to humans by comprehensive analysis of biopsies from psoriasis patients on and off anti-IL-17 treatment. Thus, dermal fibroblasts are critical for skin type 17 inflammation and represent a novel target for treatment of infection and inflammatory disease.

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IL-17 activates dermal reticular fibroblasts to promote neutrophil recruitment and host defense [RNAseq]

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