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16S rRNA sequencing of fecal samples from Atg16l1 T300A and wildtype littermate mice that were exposed to mainstream cigarette smoking co-housed with mice from the same genotype but not exposed to cigarette smoking

ABSTRACT: 16S rRNA sequencing of fecal samples from Atg16l1 T300A and wildtype littermate mice that were exposed to mainstream cigarette smoking co-housed with mice from the same genotype but not exposed to cigarette smoking

PROVIDER: PRJEB20612 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1951850_1.fastq.gz	Fastqsanger.gz
	ERR1951850_2.fastq.gz	Fastqsanger.gz
	ERR1951860_1.fastq.gz	Fastqsanger.gz
	ERR1951860_2.fastq.gz	Fastqsanger.gz
	ERR1951870_1.fastq.gz	Fastqsanger.gz

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16S rRNA sequencing of fecal samples from Atg16l1 T300A and wildtype littermate mice that were exposed to mainstream cigarette smoking co-housed with mice from the same genotype but not exposed to cigarette smoking

Project description:We found that mainstream cigarette smoking (4 cigarettes/day, 5 days/week for 2 weeks using Kentucky Research Cigarettes 3R4F) resulted in >20% decrease in the percentage of normal Paneth cell population in Atg16l1 T300A mice but showed minimal effect in wildtype littermate control mice, indicating that Atg16l1 T300A polymorphism confers sensitivity to cigarette smoking-induced Paneth cell damage. We performed cohousing experiments to test if Paneth cell phenotype is horizontally transmissible as is microbiota. Atg16l1 T300A and littermate controls that were exposed to cigarette smoking were used as microbiota donors, and these donor mice were exposed to smoking for 2 weeks prior to cohousing. Separate groups of Atg16l1 T300A and littermate controls that were not exposed to cigarette smoking were used as microbiota recipients. The microbiota recipients were co-housed with microbiota donors of the same genotype for 4 weeks, during this period the donors continued to be exposed to cigarette smoking. Cigarette smoking was performed using smoking chamber with the dosage and schedule as described above. At the end of the experiment, the fecal microbiota composition was analyzed by 16S rRNA sequencing.

2018-10-31 | E-MTAB-5720 | biostudies-arrayexpress

16S rRNA sequencing of fecal samples from Atg16l1 T300A and wildtype littermate mice that were either exposed or not to mainstream cigarette smoking for 6 weeks

2018-10-31 | E-MTAB-5717 | biostudies-arrayexpress

RNA-seq of full thickness small intestine from Atg16l1 T300A and wildtype littermate mice that were either exposed or not with mainstream cigarette smoking for 6 weeks

Project description:We found that mainstream cigarette smoking (4 cigarettes/day, 5 days/week for 6 weeks using Kentucky Research Cigarettes 3R4F) resulted in >20% decrease in the percentage of normal Paneth cell population in Atg16l1 T300A mice but showed minimal effect in wildtype littermate control mice, indicating that Atg16l1 T300A polymorphism confers sensitivity to cigarette smoking-induced Paneth cell damage. We performed transcriptional profiling to identify molecular mechanisms associated with Paneth cell defect in Atg16l1 T300A mice exposed to cigarette smoking. Female mice were used at 4-5 weeks of age. Cigarette smoking was performed using smoking chamber with the dosage and schedule as described above. The whole ileum of the mice were harvested for transcriptomic analysis after completing 6 weeks of smoking.

2018-10-31 | E-MTAB-5707 | biostudies-arrayexpress

Microarray of laser capture microdissected Paneth cells from Atg16l1 T300A and wildtype littermates mice that were either exposed or not with mainstream cigarette smoking for 6 weeks

Project description:We found that mainstream cigarette smoking (4 cigarettes/day, 5 days/week for 2 weeks using Kentucky Research Cigarettes 3R4F) resulted in >20% decrease in the percentage of normal Paneth cell population in Atg16l1 T300A mice but showed minimal effect wildtype littermate control mice, indicating that Atg16l1 T300A polymorphism confers sensitivity to cigarette smoking-induced Paneth cell damage. We performed transcriptional profiling to identify molecular mechanisms associated with Paneth cell defect in Atg16l1 T300A mice exposed to cigarette smoking. Female mice were used at 4-5 weeks of age. Cigarette smoking was performed using smoking chamber with the dosage and schedule as described above. The Paneth cells of the mice were harvested by laser capture microdissection for transcriptomic analysis after completing 6 weeks of smoking.

2018-10-31 | E-MTAB-6168 | biostudies-arrayexpress

16S rRNA sequencing of fecal samples from Atg16l1 T300A and wildtype littermate mice that were either exposed or not to mainstream cigarette smoking for 6 weeks

Project description:16S rRNA sequencing of fecal samples from Atg16l1 T300A and wildtype littermate mice that were either exposed or not to mainstream cigarette smoking for 6 weeks

| PRJEB20611 | ENA

Cigarette smoking prolongs immune responses against influenza and delays its clearance in mice

Project description:Introduction Epidemiological studies have shown that smoking is associated with increased incidence of severe viral infections leading to hospitalisation. Moreover, studies in experimental models have identified impaired antiviral responses and altered inflammatory responses, yet it is unclear which immune cells are involved and whether this varies over the course of infection. Methods To test how cigarette smoking affects the response to influenza viral infection over time, female BALB/c mice were exposed to cigarette smoke or air twice a day for 24-28 days and infected with H3N2 influenza or mock infection on day 21. Three and seven days after infection, changes in immune cell populations, and mRNA expression/viral clearance in lung tissue were analysed. Results Smoke-exposed mice lost significantly more weight than air-exposed controls after influenza infection, indicating that smoking resulted in more severe disease. Immune cell and lung tissue transcriptome analysis revealed that neutrophil infiltration was prolonged and macrophage activation dysregulated after infection in smoke-exposed mice compared to air-exposed controls. Expression of genes in IL-6 and interferon pathways was similarly longer active. In parallel, we observed lower clearance of viral RNA in smoke-exposed mice after infection compared to air-exposed controls, indicating ineffective antiviral responses. Adaptive immune responses were unchanged in infected smoking animals compared to nonsmoking mice. Conclusion Altogether, the data from our mouse model indicate that cigarette smoke exposure prolongs innate immune responses against influenza. The results from this study help to explain the susceptibility of current smokers to severe influenza disease.

2024-06-21 | GSE269227 | GEO

RNA-seq of full thickness small intestine from Atg16l1 T300A and wildtype littermate mice that were either exposed or not with mainstream cigarette smoking for 6 weeks

Project description:RNA-seq of full thickness small intestine from Atg16l1 T300A and wildtype littermate mice that were either exposed or not with mainstream cigarette smoking for 6 weeks

| PRJEB20572 | ENA

Wistar rat model of COPD: Cigarette smoking exposure and fine particulate matter (PM2.5) exposure vs. control.

Project description:Genome-wide analysis of lncRNA expression profiles in COPD rat model exposed by cigarette smoking (CS) and fine particulate matter (PM2.5). Goal was to explore the differences and similarities lncRNAs expression in rats model of COPD exposed by CS and PM2.5.

2021-06-21 | GSE178513 | GEO

Transcriptomics in response to cigarette smoking in humans

Project description:Transcriptomic analysis of the effects of cigarette smoking on the gene expression in blood in humans

2012-10-01 | GSE23323 | GEO

Cigarette smoking effect on pancreatic duct epithelial cells

Project description:Analysis of different expression of microRNAs in immortalized human pancreatic duct epithelial cells treated with cigarette smoke condensate. Cigarette smoking plays vital role in tumorigenesis and development of pancreatic ductal adenocarcinoma. Results provide insight in the machenisms involved in PDAC initiation and progression.

2019-03-24 | GSE103994 | GEO

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