ABSTRACT: Gastrointestinal colonization of Candida albicans increased serum (1--3)-beta-D-glucan, without candidemia, and worsened cecal ligation and puncture sepsis in murine model
Project description:Gastrointestinal colonization of Candida albicans increased serum (1--3)-beta-D-glucan, without candidemia, and worsened cecal ligation and puncture sepsis in murine model Metagenome
Project description:The CS and CLP murine models of intra-abdominal sepsis have unique transcriptomic respones 2 hrs, 1 and 3 days after sepsis We used mouse microarrays to detail the molecular profile of the events that occur following infection in two different sepsis models Infection protocol: Used the Cecal Ligation and Puncture (CLP) model and Cecal Slurry (CS) method in young mice.
Project description:aD is one of the b2 integrin family members. The role of aD in sepsis has not been examined yet. aD is previously reported to be expressed on neutrophils. We performed cecal ligation and puncture sepsis model in wild type and aD knockout and examined the role of aD in neutrophils.
Project description:We systematically assessed the transcriptomic changes of livers of MxCreFthD/D vs. Fthlox/lox mice after induction of polymicrobial sepsis using Cecal Ligation and Puncture. Data indicates a distinct set of genes differentially regulated between MxCreFthD/D and Fthlox/lox mice after sepsis induction reflecting altered iron and glucose metabolism.
Project description:To investigate the role of TSPO in the sequelae of sepsis induced by cecal ligation and puncture (CLP), hippocampal gene expression changes after CLP surgery were examined in wild-type and TSPO KO mice
Project description:Gene expression profiling was performed in lung tissues from an animal model of sepsis challenged with injurious and non-injurious mechanical ventilation to unravel the molecular pathways involved in acute lung injury. Sepsis was induced in male Sprague Dawley rats by means of cecal ligation and puncture. Septic rats were randomly allocated to three distinct groups: spontaneous breathing, mechanically ventilated with high tidal volume with zero positive end expiratory pressure (PEEP) and with low tidal volume and 10 cmH2O of PEEP. Comparisons were performed against an unventilated control group.
Project description:Sepsis, a worldwide health crisis, is notorious for its high mortality rate, often attributed to the development of acute lung injury. The direct migration of intestinal immune cells to the lung as a mediator of acute lung injury remains unclear. Our study unveiled a process where cecal ligation and puncture-induced sepsis prompted a migration of γδT cells from the small intestine to the lung, subsequently triggering an overwhelming inflammatory response dominated by IL-17A.
Project description:Sepsis, a worldwide health crisis, is notorious for its high mortality rate, often attributed to the development of acute lung injury. The direct migration of intestinal immune cells to the lung as a mediator of acute lung injury remains unclear. Our study unveiled a process where cecal ligation and puncture-induced sepsis prompted a migration of γδT cells from the small intestine to the lung, subsequently triggering an overwhelming inflammatory response dominated by IL-17A.
Project description:Aim: To explore the potentially important role of circulating miRNAs in systemic inflammation during sepsis. Method: 8 to 10-week old C57BL/6 mice underwent cecal ligation and puncture (CLP) or laparotomy (Sham). Plasma RNA was isolated using Trizol LS reagent 24h post-surgery. NGS cDNA libraries were prepared using Norgen Biotek Small RNA Library Prep Kit. Library quality was validated prior to sequencing on an Illumina NextSeq 500 platform.
Project description:Mesenchymal stem cells (MSCs) have shown therapeutic potential in preclinical sepsis models, but the mechanisms remain unclear. Using a murine cecal ligation and puncture model, we performed single-cell RNA sequencing of CD45+ immune cells 6 hours after MSC administration. MSC treatment improved survival and induced transcriptional reprogramming of macrophages toward an M2-like phenotype, accompanied by reduced inflammatory signatures. These findings provide mechanistic insight into MSC-mediated immune modulation in sepsis.