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Recombinant GM-CSF enhances the bactericidal ability of PMNs by increasing intracellular IL-1β and improves the prognosis of secondary Pseudomonas aeruginosa pneumonia in sepsis

ABSTRACT: Recombinant GM-CSF enhances the bactericidal ability of PMNs by increasing intracellular IL-1β and improves the prognosis of secondary Pseudomonas aeruginosa pneumonia in sepsis

PROVIDER: PRJNA943493 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23821556_1.fastq.gz	Fastqsanger.gz
	SRR23821556_2.fastq.gz	Fastqsanger.gz
	SRR23821557_1.fastq.gz	Fastqsanger.gz
	SRR23821557_2.fastq.gz	Fastqsanger.gz
	SRR23821558_1.fastq.gz	Fastqsanger.gz

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Recombinant GM-CSF enhances the bactericidal ability of PMNs by increasing intracellular IL-1β and improves the prognosis of secondary Pseudomonas aeruginosa pneumonia in sepsis

Project description:This study tested the hypothesis that recombinant granulocyte-macrophage colony-stimulating factor (rGM-CSF) enhances polymorphonuclear neutrophils (PMNs) via IL-1β to improve the prognosis of secondary infection in sepsis. The latter stage of sepsis is prone to induce immunosuppression, resulting in secondary fatal infections. rGM-CSF has become a way for sepsis-induced immunosuppression due to its immunomodulatory effect. However, the functional impact of GM-CSF on PMNs in sepsis remains obscure. This study aimed to study the role of rGM-CSF on the bactericidal ability of PMNs in septic mice, assessing its effect on the prognosis of secondary pneumonia, and explore the mechanism of rGM-CSF by intervening PMNs in patients with sepsis. The C57BL/6J sepsis mouse model was induced by cecal ligation and puncture (CLP). rmGM-CSF was used in vivo when mice developed immunosuppression, which was characterized by abnormal bactericidal function of PMNs in peripheral blood. rmGM-CSF improved the prognosis of secondary pneumonia and reversed the function of PMNs. PMNs isolated by Percoll from septic patients were treated by rhGM-CSF in vitro. The expression of CD11b, reactive oxygen species (ROS), phagocytosis and neutrophil extracellular traps (NETs) release in PMNs were enhanced by rhGM-CSF treatments. Whole-transcriptomic sequencing of mouse PMNs indicated that recombinant GM-CSF increased the expression of il1b gene in PMNs. Blocking and inhibiting IL-1β release effectively counteracted the enhancing effect of GM-CSF on the bactericidal function of PMNs. RmGM-CSF enhances the bactericidal function of PMNs in vivo and improves the prognosis of secondary pneumonia in septic mice, and recombinant GM-CSF increases IL-1β precursor reserves, which, if stimulated, can rapidly enhance the bactericidal capacity of PMNs.

2024-03-01 | GSE227162 | GEO

Genome-wide analysis expression of ileum samples from PGC-1β fl/? and iKOPGC-1β

Project description:Analysis of metabolic pathway gene expression. The hypothesis tested in the present study is to assess mRNA level changes in metabolic genes in enterocytes from intestine specific PGC-1β konckout mice. Total RNA obtained from ileum samples from IKOPGC-1β mice was compared to the total RNA extracted from their wild-type littermates.

2015-03-01 | E-GEOD-61640 | biostudies-arrayexpress

Analysis of Metabolically Stressed Primary Hepatocytes with IL-1β Recombinant Protein for 24 Hours

Project description:RNA-seq analysis of primary hepatocytes isolated from C57BL/6N mice, stimulated with IL-1β recombinant protein to examine the transcriptional response to inflammatory signaling.

2025-03-12 | GSE282137 | GEO

Sublytic concentrations of Staphylococcus aureus Panton-Valentine leukocidin alter human polymorphonuclear leukocyte gene expression and enhance bactericidal capacity.

Project description:Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) infections are often caused by strains encoding Panton-Valentine leukocidin (PVL). PVL can cause lysis of polymorphonuclear leukocytes (PMNs) and other myeloid cells in vitro, a function considered widely as the primary means by which PVL might contribute to disease. However, at sublytic concentrations PVL can function as a PMN agonist. To better understand this phenomenon, we investigated the ability of PVL to alter human PMN function. PMNs exposed to PVL had enhanced capacity to produce superoxide in response to N-formyl-methionyl-leucyl-phenylalanine (fMLF), but unlike priming by lipopolysaccharide, this response did not require Toll-like receptor signal transduction. On the other hand, there was subcellular redistribution of NADPH oxidase components in PMNs following exposure of these cells to PVL - a finding consistent with priming. Priming of PMNs with other agonists such as IL-8 or GM-CSF altered the ability PVL to cause formation of pores in the plasma membranes of these cells. Microarray analysis revealed significant changes in the human PMN transcriptome following exposure to PVL, including up-regulation of molecules that regulate the inflammatory response. Consistent with the microarray data, mediators of the inflammatory response were released from PMNs after stimulation with PVL. We conclude that exposure of human PMNs to sublytic concentrations of PVL elicits a proinflammatory response that is regulated in part at the level of gene expression. We propose that PVL-mediated priming of PMNs enhances the host innate immune response.

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Hnf-1β ChIP-Seq

Project description:Genome Wide mapping of Hnf-1β in kidney cells. Tissue-specific transcription factor that is expressed in the kidney and other epithelial organs. Humans with mutations in HNF1? develop kidney cysts, and HNF-1β regulates the transcription of several cystic disease genes. However, the complete spectrum of HNF-1β-regulated genes and pathways is not known. Here, we used ChIP-seq and DNA microarray analysis to identify 1,545 protein-coding genes that are directly regulated by HNF-1β in kidney epithelial cells. Pathway analysis predicted that HNF-1β regulates cholesterol metabolism. The expression of genes that are essential for cholesterol synthesis, including Srebf2 and Hmgcr, was reduced by expression of dominant-negative mutant HNF-1β or kidney-specific inactivation of HNF-1β. The levels of cholesterol biosynthetic intermediates and the rate of cholesterol synthesis were decreased in HNF-1β mutant cells. In addition, HNF-1β directly regulated the renal epithelial expression of PCSK9, a key regulator of cholesterol uptake, and depletion of cholesterol in the culture medium mitigated the inhibitory effects of mutant HNF-1β on SREBP-2 and HMGCR. These findings reveal a novel role of HNF-1β in regulating multiple steps in renal cholesterol metabolism.

2015-08-15 | GSE71250 | GEO

Pneumonia-induced shedding of epithelial heparan sulfate inhibits the bactericidal activity of cathelicidin

Project description:Pneumonia-induced shedding of epithelial heparan sulfate inhibits the bactericidal activity of cathelicidin

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NIH/NIAID GM-CSF Modulates Global Changes in Neutrophil Gene Expression

Project description:PMNs were isolated from venous blood of healthy individuals in accordance with a protocol approved by the Institutional Review Board for Human Subjects, National Institute of Allergy and Infectious Diseases. Human PMNs (107) were cultured in RPMI/H -/+ 100 ng/ml GM-CSF at 37oC and 5% CO2 for up to 24 h as indicated. At the indicated time points, tissue culture medium was aspirated from each well and PMNs were lysed with RLT buffer (Qiagen). Purification of PMN RNA and subsequent preparation of labeled cRNA target was performed as described in Methods. Labeling of samples, GeneChip hybridization (Hu95Av2 oligonuceotide microarrays) and scanning were performed according to standard Affymetrix protocols (see http://www.affymetrix.com/support/technical/manual/expression_manual.affx). Experiments were performed in triplicate, using PMNs from three healthy individuals for each treatment. These analyses allowed comparison of global gene expression in human neutrophils during spontaneous apoptosis with that in cells cultured with human GM-CSF. Keywords: time course

2005-10-07 | GSE2803 | GEO

Sublytic concentrations of Staphylococcus aureus Panton-Valentine leukocidin alter human polymorphonuclear leukocyte gene expression and enhance bactericidal capacity.

2012-09-06 | E-GEOD-33939 | biostudies-arrayexpress

Prenylcysteine oxidase 1 like protein is required for neutrophil bactericidal activities

Project description:The bactericidal function of neutrophils are dependent on myriad intrinsic and extrinsic stimuli. Using systems immunology approaches we identified microbiome- and infection-induced changes in neutrophils. We focused on investigating the Prenylcysteine oxidase 1 like (Pcyox1l) protein function. Murine and human Pcyox1l proteins share ninety four percent aminoacid homology revealing significant evolutionary conservation and implicating Pcyox1l in mediating important biological functions. Here we show that the loss of Pcyox1l protein results in significant reductions in the mevalonate pathway impacting autophagy and cellular viability under homeostatic conditions. Concurrently, Pcyox1l CRISPRed-out neutrophils exhibit deficient bactericidal properties. Pcyox1l knock-out mice demonstrate significant susceptibility to infection with the gram-negative pathogen P. aeruginosa exemplified through increased neutrophil infiltrates, hemorrhaging, and reduced bactericidal functionality. Cumulatively, we ascribe a function to Pcyox1l protein as a fundamental regulator of the prenylation pathway and suggest connections beween metabolic responses and neutrophil functionality. Anastasia Petenkova , Shelby A. Auger, Jeffrey Lamb, Daisy Quellier, Cody Carter, On TakTo, Jelena Milosevic, Rana Barghout, Abirami Kugadas, Xiaoxiao Lu, Jennifer Geddes-McAlister, Raina Fichorova, David B. Sykes, Mark D. Distefano, and Mihaela Gadjeva. 2023. Prenylcysteine oxidase 1 like protein is required for neutrophil bactericidal activities. Nat.Comm.

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2022-07-19 | E-MTAB-11887 | biostudies-arrayexpress

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