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Candida albicans-infected mice increased bacterial sepsis severity

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

PROVIDER: PRJNA369313 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5223766_1.fastq.gz	Fastqsanger.gz
	SRR5223766_2.fastq.gz	Fastqsanger.gz

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Candida albicans-infected mice increased bacterial sepsis severity

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

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Host Responses to Sepsis Vary in Different Low-Lethality Murine Models

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.

2014-02-21 | E-GEOD-55238 | biostudies-arrayexpress

The role of aD in sepsis

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.

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The role of ferritin heavy chain (Fth) in polymicrobial sepsis.

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.

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Gut-derived memory γδ T17 cells exacerbate sepsis-induced acute lung injury [scRNA-seq]

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.

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Gut-derived memory γδ T17 cells exacerbate sepsis-induced acute lung injury [ChIP-seq]

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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.

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Plasma circulating miRNA profiling in polymicrobial sepsis by high throughput sequencing

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Sepsis gene expression profiling: murine splenic compared with hepatic responses

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