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myeloid cells

GPR84 Signaling Promotes Intestinal Mucosal Inflammation via Enhancing NLRP3 Inflammasome Activation in Macrophages

[Acta Pharmacologica Sinica] Scientists demonstrated that GPR84 was highly upregulated in inflamed colon tissues of active ulcerative colitis patients and dextran sulfate sodium-induced colitis mice.

Molecular Drivers of Tumor Progression in Microsatellite Stable APC Mutation-Negative Colorectal Cancers

[Scientific Reports] Scientists analyzed data from The Cancer Genome Atlas to compare clinical phenotypes, somatic mutations, copy number variations, gene fusions, RNA expression, and DNA methylation profiles between APCmut– and APC mutation-positive (APCmut+) microsatellite stable colorectal cancer cells.

Directly Recruited GATA6 + Peritoneal Cavity Macrophages Contribute to the Repair of Intestinal Serosal Injury

[Nature Communications] Researchers showed, using spinning-disk confocal microscopy, that large F4/80hiGATA6+ peritoneal cavity macrophages promptly accumulate at damaged intestinal sites upon intestinal thermal injury and upon dextran sodium sulfate induced colitis in mice via a direct route from the peritoneal cavity.

Bruton’s Tyrosine Kinase (BTK) Regulates Myeloid Cell Recruitment during Acute Inflammation

[British Journal of Pharmacology] Investigators explored the role of BTK on the migration of myeloid cells; in vitro using chemotaxis assays and in vivo using zymosan induced peritonitis as model systems.

Glutathione Synthesis Primes Monocytes Metabolic and Epigenetic Pathway for β-Glucan-Trained Immunity

[Redox Biology] Researchers reported that β-glucan-trained macrophages from mice harboring a myeloid-specific deletion of the catalytic subunit of glutamate-cysteine ligase showed impaired GSH synthesis and decreased proinflammatory cytokine production in response to lipopolysaccharide challenge.

Reduction of NETosis by Targeting CXCR1/2 Reduces Thrombosis, Lung Injury, and Mortality in Experimental Human and Murine Sepsis

[British Journal of Anaesthesia] Scientists quantified ex vivo neutrophil extracellular traps (NET) induction in septic humans and murine models of sepsis to identify signalling pathways that may be modulated to improve outcome in human sepsis.

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