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Transcriptomic analysis of the Pseudomonas sp. AP3_22 exposed to the sodium dodecyl sulfate

ABSTRACT: Transcriptomic analysis of the Pseudomonas sp. AP3_22 exposed to the sodium dodecyl sulfate

PROVIDER: PRJNA434001 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6723860_1.fastq.gz	Fastqsanger.gz
	SRR6723860_2.fastq.gz	Fastqsanger.gz
	SRR6723870_1.fastq.gz	Fastqsanger.gz
	SRR6723870_2.fastq.gz	Fastqsanger.gz
	SRR6723880_1.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis of the Pseudomonas sp. AP3_22 exposed to the sodium dodecyl sulfate

Project description:Here we presented the detailed transcriptomic analysis for Pseudomonas sp. AP3_22, an effective sodium dodecyl sulfate degrader isolated from the soil sample from wastewater treatment plant, cultured in the presence of SDS to get the first insight in the global bacterial response toward Sthis anionic detergent. Our results suggest showed that although SDS could be used as a carbon source, in the first place it acts influence on integrity of the cell envelopes and causes global stress response together combined with cell wall modification and repair induction. These results suggest that the modulation of the membrane content composition is first adaptation step in a typical response to detergent exposure. As the second response to the sodium dodecyl sulfate the AP3_22 strain metabolism was shifted from the lipid biosynthesis to the lipid catabolism and the SDS degradation started.

2018-05-01 | GSE110573 | GEO

Transcriptomic fingerprints of C. elegans exposed to sodium perchlorate.

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Whole ileal tissue from day 6 Dextran Sodium Sulfate (DSS) administered Il17rafl/fl;Atoh1-cre+/- mice

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Dextran sodium sulfate treatment of Pirc rats alters colonic and tumor gene expression

Project description:Dextran sodium sulfate (DSS) causes inflammation in the gut similar to ulcerative colitis in humans. Patients with ulcerative colitis have increased risk of developing colon cancer. We sought to determine whether genes altered in the normal colonic epithelium or tumor differed between sporadic and inflammation-associated tumor development.

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The reduction of dextran sulfate sodium-induced colitis severity in mice exposed to cigarette smoke is accompanied by specific gene pathway and microbial shifts.

Project description:Background and Aims: The impact of cigarette smoke on inflammatory bowel disease has been established by a large number of epidemiological, clinical, and preclinical studies. Exposure to cigarette smoke is associated with a higher risk of developing Crohn’s disease but is inversely correlated with the development, disease risks, progression, and relapse rate of ulcerative colitis. Few mechanistic studies have investigated the effect of cigarette smoke on intestinal inflammation and microbial composition. Methods: Three groups of mice were exposed to three different concentrations of cigarette smoke for a total of 4 weeks, including 5 days of dextran sulfate sodium treatment to induce colitis and a 7-day recovery period. A comprehensive and integrated comparative analysis of the global colon transcriptome and microbiome, as well as classical endpoints, was performed. Results: Cigarette smoke exposure significantly decreased the severity induced colitis. Colon transcriptome analysis revealed that cigarette smoke downregulated specific pathways in a concentration-dependent manner, affecting both the inflammatory state and composition of the gut microbiome. Metagenomics analysis demonstrated that cigarette smoke can modulate dextran sulfate sodium-induced dysbiosis of specific bacterial genera, contributing to resolve the inflammation or accelerate recovery. Conclusions: Cigarette smoke alters gut microbial composition and reduces inflammatory responses in a concentration-dependent manner. The present study lays the foundation for investigating potential molecular mechanisms responsible for the attenuation of colitis by cigarette smoke.

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Project description:Dextran sodium sulfate (DSS) causes inflammation in the gut similar to ulcerative colitis in humans. Patients with ulcerative colitis have increased risk of developing colon cancer. We sought to determine which genes are altered in the normal colonic epithelium, and which changes depend on the Pirc mutation.

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