Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Neutrophil-specific defensin receptors prevent skin dysbiosis and bacterial infection

ABSTRACT: Neutrophil-specific defensin receptors prevent skin dysbiosis and bacterial infection

PROVIDER: PRJNA739453 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Neutrophil-specific defensin receptors prevent skin dysbiosis and bacterial infection

Project description:Healthy skin maintains a diverse microbiome and a potent immune system to fight off infections. In this study, we discovered that epithelium-derived antimicrobial peptides defensins activate orphan GPCRs Mrgpra2a/b on neutrophils. This signaling axis is required for effective neutrophil-mediated skin immunity and microbiome homeostasis. We generated two mutant mouse lines, Defensin conditional knockout (Def cKO, K14-cre; Def fl/fl) in which the entire Def gene cluster is conditionally deleted from keratinocytes, and Mrgpra2 double knockout (Mrgpra2 dKO). We used high-throughput RNA sequencing to evaluate the whole transcriptomes of WT and mutant animals' skin under naive condition and 24 hours post-S. aureus infection. Disruption of defensin-Mrgpra2 signaling caused reduction of a network of pro-inflammatory and antibacterial gene expression. This study demonstrates the importance of epithelial-neutrophil signaling via the defensin-Mrgpra2 axis in maintaining healthy skin ecology and promoting antibacterial host defense.

2021-10-01 | GSE178507 | GEO

Stem cell-derived neutrophil-primed progenitors prevent lethal infection

Project description:Stem cell-derived neutrophil-primed progenitors prevent lethal infection

| PRJNA658513 | ENA

Stem cell-derived neutrophil-primed progenitors prevent lethal infection

Project description:We show that engineered neutrophil-primed progenitors derived from human induced pluripotent stem cells (NeuPs-XL) can produce functional neutrophil-like cells (NeuCs-XL) that can act promptly in vivo against lethal bacterial infections at a clinically applicable scale. We performed global gene expression profiling of NeuPs-XL and NeuCs-XL with or without LPS stimulation.

2020-08-22 | GSE156612 | GEO

Fungal dysbiosis Arabidopsis roots

Project description:Tryptophan metabolism and bacterial commensals prevent fungal dysbiosis in Arabidopsis roots, Bacterial data

| PRJEB45520 | ENA

Fungal dysbiosis Arabidopsis roots

Project description:Tryptophan metabolism and bacterial commensals prevent fungal dysbiosis in Arabidopsis roots, Fungal data

| PRJEB45521 | ENA

Fungal dysbiosis Arabidopsis roots

Project description:Tryptophan metabolism and bacterial commensals prevent fungal dysbiosis in Arabidopsis roots, Oomycetal data

| PRJEB45522 | ENA

Colonic Gene expression of SPF mice fed either a Control Diet or a High Salt Diet

Project description:Compositional changes in the microbiota (dysbiosis) may be a basis for Irritable Bowel Syndrome (IBS) but biomarkers are currently unavailable to direct microbiota-directed therapy. We therefore examined whether changes in fecal β-defensin could be a marker of dysbiosis in a murine model. Experimental dysbiosis was induced using four interventions relevant to IBS: a mix of antimicrobials, westernized diets (high-fat/high-sugar and, high salt diets), or mild restraint stress. Fecal mouse β-defensin-3 and 16S rRNA-based microbiome profiles were assessed at baseline, during and following these interventions. Each intervention, except for mild restraint stress, altered compositional and diversity profiles of the microbiota. Exposure to antimicrobials or a high-fat/high-sugar diet, but not mild restraint stress, resulted in decreased fecal β-defensin-3 compared to baseline. In contrast, exposure to the high salt diet increased β-defensin-3 compared to baseline but this was not accompanied by discernible inflammatory changes in the host.

2023-07-11 | GSE225272 | GEO

Synthetic Siglec-9 agonists inhibit neutrophil activation associated with COVID-19

Project description:Severe cases of coronavirus disease 2019 (COVID-19) are characterized by a hyperinflammatory immune response that leads to numerous complications. Production of proinflammatory neutrophil extracellular traps (NETs) has been suggested to be a key factor in inducing a hyperinflammatory signaling cascade, allegedly causing both pulmonary tissue damage and peripheral inflammation. If true, finding ways to inhibit NET production could provide therapeutic strategies to prevent respiratory damage and death from SARS-CoV-2 related inflammation. Here, we demonstrate that synthetic glycopolymers that activate signaling of the neutrophil checkpoint receptor Siglec-9 suppress NETosis induced by agonists of viral TLR receptors and COVID-19 plasma. Thus, Siglec-9 represents an attractive therapeutic target to curb neutrophilic hyperinflammation in COVID-19.

2021-07-28 | PXD022990 | Pride

Effect of human beta defensin-2 (hBD-2) on T cells [mouse]

Project description:In this experiment, we studied how human beta defensin-2 (hBD-2) affects kinase activity of T cells.

2022-12-20 | GSE198404 | GEO

Effect of human beta defensin-2 (hBD-2) on T cells [human]

Project description:In this experiment, we studied how human beta defensin-2 (hBD-2) affects kinase activity of T cells.

2022-12-20 | GSE198402 | GEO