Human Induced Pluripotent Stem Cells derived Neutrophils Display Strong Anti-microbial Potencies
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1231067 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32556651_1.fastq.gz | Fastqsanger.gz | |||
| SRR32556651_2.fastq.gz | Fastqsanger.gz | |||
| SRR32556652_1.fastq.gz | Fastqsanger.gz | |||
| SRR32556652_2.fastq.gz | Fastqsanger.gz | |||
| SRR32556653_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:Neutrophils are essential innate immune cells with unusual anti-microbial properties while dysfunctions of neutrophils lead to severe health problems such as lethal infections. Generation of neutrophils from human induced pluripotent stem cells (hiPSCs) is highly promising to produce off-the-shelf neutrophils for transfusion therapies. However, the anti-microbial potencies of hiPSCs derived neutrophils (iNEUs) remain less documented. Here, we develop a scalable approach to generate iNEUs in a chemical defined condition. iNEUs display typical neutrophil characters in terms of phagocytosis, migration, formation of neutrophil extracellular traps (NETs), etc. Importantly, iNEUs display a strong killing potency against various bacteria such as K.pneumoniae, P.aeruginosa, E.coli and S.aureus. Moreover, transfusions of iNEUs in mice with neutrophil dysfunction largely enhance their survival in lethal infection of different bacteria. Together, our data show that hiPSCs derived neutrophils hold strong anti-microbial potencies to protect severe infections under neutrophil dysfunction conditions.
2025-03-26 | GSE290954 | GEO
Project description:Monocytes and neutrophils are both myeloid cells that have the same progenitor, the granulocyte macrophage precursor (GMP). Neutrophils are mature innate cells that are phagocytes and can degranulate to mount an immune response, whereas monocytes are immature pluripotent cells that can differentiate into macrophages and dendritic cells that can phagocytose and present antigen. To compare the expression pattern and validate samples purity by comparing expression data with previously generated data for monocytes and neutrophils, we isolated monocytes (CD45+ CD64+ CD14+ CD16-) and neutrophils (CD66b+ CD16+) from eight healthy volunteers.
2014-03-20 | E-MTAB-1573 | biostudies-arrayexpress
Project description:Polystyrene microplastics induce activation and cell death of neutrophils through strong adherence and engulfment
| PRJNA1235753 | ENA
Project description:Ingested microplastics (MPs) can accumulate throughout whole body, which may induce the dysfunction of immune system. However, it remains unclear how MP exposure affects innate immune responses at the cellular level. We found that mouse neutrophils strongly bind and then engulf polystyrene MPs. This interaction leads to proinflammatory state of neutrophils and eventually results in apoptotic cell death through toll-like receptor signaling pathway in a bacteria-recognition mimetic manner. Moreover, our data verified that orally administered polystyrene MPs reach various organs in mice, where they are interacted with and endocytosed by neutrophils. We confirmed that human neutrophils also strongly bind and internalize polystyrene MPs. Additionally, RNA sequencing analysis of polystyrene MPs-exposed human neutrophils showed the upregulation of cell death-related function. Therefore, the accumulated MPs may exacerbate inflammatory immune response by disrupting neutrophil function. These results provide novel insight into the adverse responses of neutrophils induced by MP exposure.
2025-03-18 | GSE291904 | GEO
Project description:This study investigated neutrophils in systemic onset Juvenile Idiopathic Arthritis (sJIA), one of the most common multifactorial autoinflammatory diseases, characterized by arthritis and severe systemic inflammatory manifestations like fever, rash, hepatosplenomegaly and serositis. Neutrophil counts were markedly increased at disease onset, correlated to levels of inflammatory mediators and normalized within days after initiation of therapy with recombinant IL-1 receptor antagonist (rIL-1RA). Neutrophils isolated from 3 sJIA patients with active disease, before initiation of therapy (2 disease onset, 1 systemic flare) and 3 healthy controls were compared. A clear separation between the transcriptome of sJIA patients and HCs was observed. In total, 1068 genes were significantly upregulated and 625 genes were downregulated in sJIA; GO-analyses indicated upregulation of inflammatory processes in sJIA neutrophils compared to HCs. GSEA analyses revealed a significant enrichment with the transcriptome of neutrophils in sepsis patients. Correspondingly, neutrophils from sJIA patients during active disease displayed a primed phenotype characterized by an increased respiratory burst, CD62L shedding and degranulation of secretory vesicles. This phenotype was completely reversed in sJIA patients in remission on rIL-1RA. Our data show an important role for neutrophils in the early inflammatory phase of sJIA and a strong susceptibility of neutrophil numbers and inflammatory activity to IL-1 signaling blockade.
2018-02-12 | GSE103170 | GEO
Project description:[Background] TNFa-induced adipose-related protein (TIARP) is a six-transmembrane protein that is expressed on macrophages, neutrophils and synoviocytes. We have recently reported that TIARP deficient mice (TIARP-/-) spontaneously developed arthritis, and had the high susceptibility to collagen-induced arthritis (CIA) with enhanced interleukin (IL)-6 production. However, the effect of TIARP to neutrophils and fibroblast-like syonoviocytes (FLS) has not been clearly elucidated. [Methods] We analyzed the roles of TIARP in K/BxN serum transfer model using TIARP-/- mice. We characterized the differences of neutrophils between WT and TIARP-/- mice by DNA microarray. Transmigration assays of TIARP-/- neutrophils were performed in vitro and in vivo. FLS were cultured with TNF? and the production of CXCL2 (a specific ligand of CXCR1 and CXCR2) and IL-6 were measured by ELISA. Moreover, TIARP-/- mice transferred with K/BxN serum were treated with anti-IL-6R antibodies. [Results] Arthritis in TIARP-/- mice transferred with K/BxN serum was significantly exacerbated. We identified overexpression of CXCR1 and CXCR2 in TIARP-/- neutrophils by DNA microarray. Neutrophils from TIARP-/- mice showed strong migration activity. The enhancement of chomotactic activity of TIARP-/- neutrophil was greatly facilitated by CXCL2 in vitro and in vivo. In addition, TIARP-/-FLS has enhanced the production of CXCL2 and IL-6 and the cell proliferation in the presence of TNFa, and the blockade of IL-6R significantly attenuated arthritis in vivo. [Conclusion] Our findings indicate that TIARP might down-regulate the production of CXCL2 and IL-6 in FLS, and the expression of chemokine receptors (CXCR1 and CXCR2) in neutrophils, resulting in the protective ability of neutrophils migration into arthritic joints. Mice were treated with thiogycollate medium intraperitoneally. After 3 days, peritoneal macrophages were isolated from three WT or TIARP-deficient mice, and these cells were stimulated by TNF? for 24 hours. Ly6G+ Neutrophils were isolated from splenocytes by MACS.
2015-09-23 | E-GEOD-73306 | biostudies-arrayexpress
Project description:Fetal neutrophils from early embryonic stages display a reduced capacity to react to inflammatory stimuli, therefore this study aimed to investigate the underlying molecular mechanisms regulating fetal neutrophil function during ontogeny. Whole transcriptome analysis of human fetal cord blood-derived neutrophils from premature (<37 weeks of gestation) and mature (>37 weeks of gestation) infants, compairing their gene expression profiles to neutrophils from healthy adult donors
2023-01-26 | GSE222156 | GEO
Project description:Our group has proposed that low-density granulocytes (LDGs) play an important role in lupus pathogenesis, as they can damage endothelial cells and synthesize increased levels of proinflammatory cytokines and type I interferons. LDGs have a heightened capacity to synthesize neutrophil extracellular traps (NETs). NETs from LDGs display increased levels of bactericidal and immunostimulatory proteins, such as the cathelicidin LL37 and externalize double-stranded DNA (dsDNA). Lupus netting LDGs have increased capacity to kill endothelial cells and expose IL-17. Through NETosis, lupus neutrophils stimulate plasmacytoid DCs to synthesize IFN-?. Our results further expand the potential pathogenic role of aberrant lupus neutrophils through a NET-mediated effect. We used microarrays to analyze the gene expression of neutrophils in healthy and lupus patients, and of low-density granulocytes in lupus patients. Human neutrophils and LDGs were isolated from PBMCs. RNA from healthy neutrophils, lupus neutrophils and lupus LDGs was extracted and processed for hybridization on Affymetrix microarrays.
2011-06-22 | E-GEOD-26975 | biostudies-arrayexpress
Project description:Neutrophils are key players in the hyperinflammatory response during SARS-CoV-2 infection, exhibiting features of deregulation and reprogramming. The cytosolic proliferating cell nuclear antigen (PCNA) is a scaffolding protein highly dependent on the microenvironment status and known to interact with numerous proteins that regulate neutrophil survival, NADPH oxidase-dependent reactive oxygen species (ROS) production, and cell energy metabolism. In this sense this study aimed to examine the cytosolic protein content and PCNA interactome in neutrophils from COVID-19 patients. Methods: Proteomics analysis was performed on neutrophil cytosols from healthy donors and patients with severe or critical COVID-19. In vitro approaches with ultrapure neutrophils were employed to validate the role of PCNA dynamics in neutrophil overactivation during COVID-19.
2025-05-07 | PXD055810 | Pride
Project description:Tumor infiltrating neutrophils (TAN) have been shown to exert both pro- and anti-tumoral activities and their recruitment and polarization are triggered by tumor-derived signals. Resident mesenchymal stromal cells (MSC) could contribute to tumor-supportive cell niche and have been shown to display tumor-specific transcriptomic, phenotypic, and functional features compared to normal tissue. In our study, we investigate whether these two cell subsets establish a bidirectional crosstalk in the context of B-cell lymphoma. We used microarrays to explore how neutrophils could trigger the polarization of tumor-supportive stromal cells. Gene expression analysis were performed on stromal cells (MSC) derived from bone marrow (BM) or tonsil (Resto) of healthy donors. These BM-MSC (n=3) or Resto (n=3) were primed or not with neutrophils for 1 day to induce stromal modification.
2015-05-11 | E-GEOD-62782 | biostudies-arrayexpress