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Thermoneutral housing regulates intestinal tissue tolerance

ABSTRACT: Thermoneutral housing regulates intestinal tissue tolerance

PROVIDER: PRJNA665457 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12703562.fastq.gz	Fastqsanger.gz
	SRR12703563.fastq.gz	Fastqsanger.gz
	SRR12703564.fastq.gz	Fastqsanger.gz
	SRR12703565.fastq.gz	Fastqsanger.gz
	SRR12703566.fastq.gz	Fastqsanger.gz

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Thermoneutral housing regulates intestinal tissue tolerance

Project description:Purpose: Tissue tolerance is a host defense strategy that protects tissues from damage cuased by pathogens or the immune system. Here, we provide a framework for investigating the mechanisms of tissue tolerance in experimental models of colitis. We find that the program of tissue tolerance is preferentially expressed in thermoneutral mice, which protects them from injury-induced colitis and inflammation-induced colon cancer. The expression of intestinal tissue tolerance is mediated by an unexpected crosstalk between thermogenic adipocytes and intestinal epithelial cells.

2020-09-25 | GSE158488 | GEO

Effect of thermoneutral housing on non-alcoholic fatty liver disease in mice

Project description:Purpose: To identify the impact of thermoneutral housing as opposed to standard housing on gene expression profiles in the mouse peripheral blood mononuclear cells (PBMCs), focusing on proinflammatory immune responses and high-fat diet induced non-alcoholic fatty liver disease pathogenesis. Methods: Expression profiles from PBMCs collected from C57Bl6 mice fed chow or high-fat diet for 8 weeks, following 2 weeks at either standard or thermoneutral housing conditions. Sequencing was performed in duplicate, the Illumina HiSeq 2500. Transcripts that passed quality filters were analyzed at the gene level, using Strand NGS for accurate alignment and quantification. Results: We mapped approximately 20million reads per sample to the mm10 genome using annotations produced by Ensembl, which represented 36186 transcripts. Approximately 14000 genes exhibited reasonable expression in at least one experimental condition. The primary focus was the effect of housing temperature while holding diet consistent (i.e. thermoneutral vs standard, both on high-rat diet), where ~2700 genes exhibited differential regulation. Conclusions: We present the transcriptomic profile of PBMCs from mice fed chow of high-fat diets, following either standard or thermoneutral housing. We obseve an augmented proinflammatory immune response.

2017-02-12 | GSE80976 | GEO

Adaptation of white adipose tissue to cool environmental temperatures

Project description:To map changes in RNAs that occur to the gluteal portion of the posterior subcutaneous adipose tissue of mice housed under cool temperature, we performed RNA-Seq on gluteal WAT of mice housed at 22°C compared with thermoneutral housing (29°C; control).

2021-04-28 | GSE169142 | GEO

HIF2 regulates intestinal Wnt5a expression

Project description:HIF2 regulates intestinal Wnt5a expression

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Effect of housing condition (group- or single-housing) on gene expression in African turquoise killifish II.

Project description:To explore the effects of the housing condition (group- or single-housing) on killifish, we performed RNA-seq analysis for the whole bodies of male and female juveniles, gonads of males and females from puberty to middle age, and livers of young and old males.

2024-10-13 | GSE245481 | GEO

Effect of housing condition (group- or single-housing) on gene expression in African turquoise killifish I.

2024-10-13 | GSE245480 | GEO

Malat1 regulates intestinal epithelial cell function

Project description:The long-non-coding RNA Malat1 is abundantly expressed in all subsets of the intestinal epithelial cells (IEC). Here, we compared the transcriptome of the small intestinal and colonic epithelium of wildtype and Malat1-/- mice under steady state. We found that Malat1 is involved in IEC homeostasis, intestinal microbial balance, and regulates programs involved in intestinal cancer.

2023-04-28 | GSE208232 | GEO

The intestinal microbiota regulates body composition through NFIL3 and the circadian clock

Project description:The intestinal microbiota has been identified as an environmental factor that markedly impacts energy storage and body fat accumulation, yet the underlying mechanisms remain unclear. Here we show that the microbiota regulates body composition through the circadian transcription factor NFIL3. Nfil3 transcription oscillates diurnally in intestinal epithelial cells and the amplitude of the circadian oscillation is controlled by the microbiota through type 3 innate lymphoid cells (ILC3), STAT3, and the epithelial cell circadian clock. NFIL3 controls expression of a circadian lipid metabolic program and regulates lipid absorption and export in intestinal epithelial cells. These findings provide mechanistic insight into how the intestinal microbiota regulates body composition and establish NFIL3 as an essential molecular link among the microbiota, the circadian clock, and host metabolism.

2017-09-26 | GSE100339 | GEO

Effect of thermoneutral housing conditions on the hepatotoxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in male C57BL/6 mice

Project description:Typical rodent toxicology experiments are performed at human thermoneutral temperatures (thermostandard; TS = 20 – 24° C). Reports have indicated that investigation of metabolic endpoints at mouse thermoneutral temperatures (TNM = 28 – 30° C) improves translation to humans when they are not chronically cold-stressed. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has been shown to dose-dependently induce metabolic disease in mice at including liver steatosis, steatohepatitis, and periportal fibrosis. To test whether dose-dependent hepatotoxicity caused by TCDD is altered by housing temperature we gavaged male C57BL/6 mice every 4 days for 28 days with TCDD (0.03 – 30 µg/kg) or sesame oil vehicle at TS and TNM. Mice held at TNM exhibited less marked relative liver weight gain and histopathology with milder steatosis, immune cell infiltration, hepatocellular hypertrophy, and an absence of biliary hyperplasia compared to mice held at Ts. Mice housed in both temperature conditions had a similar dose-dependent decrease in total cholesterol, but mice at TS had more elevated serum ALT and decreased glucose and triglycerides at 30 µg/kg TCDD. Mice at TNM had fewer differentially expressed genes (DEGs) than TS, although most of the DEGs at TNM were shared with the DEGs at TS. Benchmark Dose (BMD) analysis performed on the DEGs revealed largely similar trends, however, the most induced DEGs, which constituted some of the AhR-battery genes (e.g. Cyp1a1), exhibited lower BMDs at TNM. Moreover, at 30 µg/kg TCDD both sets of mice had increased pro-inflammatory cytokines. The only cytokine which was clearly different between the two sets of mice irrespective of dose was VEGF-A. Overall, mice held at TNM showed reduced severity at equivalent doses to mice held at TS.

2023-09-18 | GSE203300 | GEO

Enteric pathogens induce tissue tolerance and prevent neuronal loss from subsequent infections

Project description:The enteric nervous system (ENS) controls several intestinal functions including motility and nutrient handling, which can be disrupted by infection-induced neuropathies or neuronal cell death. We investigated possible tolerance mechanisms preventing neuronal loss and disruption in gut motility after pathogen exposure. We found that following enteric infections, muscularis macrophages (MMs) acquire a tissue-protective phenotype that prevents neuronal loss and dysmotility during subsequent challenge with unrelated pathogens. Bacteria-induced neuroprotection relied on activation of gut-projecting sympathetic neurons and signaling via b2-adrenergic receptors (b2AR) on MMs. In contrast, helminth-mediated neuroprotection was dependent on T cells and systemic production of interleukin (IL)-4 and -13 by eosinophils, which induced arginase-expressing MMs that prevented neuronal loss from an unrelated infection located in a different intestinal region. Collectively, these data suggest that distinct enteric pathogens trigger a state of disease- or tissue tolerance that preserves ENS number and functionality.

2021-08-17 | GSE182294 | GEO

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