Thermoneutral housing regulates intestinal tissue tolerance
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA665457 | ENA |
REPOSITORIES: ENA
Dataset's files
| 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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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
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
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
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
Project description:Effect of thermoneutral housing conditions on the hepatotoxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in male C57BL/6 mice
| PRJNA839384 | ENA
Project description:Interplay between parenchymal energy-storing white adipose cells and thermogenic beige adipocytes contributes to obesity and insulin resistance. Irrespective of cellular origin or specialized niche, adipocytes require the activity of the nuclear receptor peroxisome proliferator activated receptor gamma (PPARγ) for proper function. Exposure to cold or adrenergic signaling enriches thermogenic cells though multiple pathways that act synergistically with PPARγ, however, the molecular mechanisms by which PPARγ licenses white adipose tissue (WAT) to preferentially adopt a thermogenic or white adipose fate in response to dietary cues or thermoneutral conditions are not fully elucidated. Here, we show that a PPARγ-long noncoding RNA (lncRNA) axis integrates canonical and noncanonical thermogenesis to restrain white adipose tissue heat dissipation during thermoneutrality and diet-induced obesity (DIO). Pharmacologic inhibition or genetic deletion of the lncRNA Lexis, enhances UCP-1 dependent and independent thermogenesis. Adipose tissue specific deletion of Lexis counteracted diet-induced obesity, improved insulin sensitivity, and enhanced energy expenditure. Single-nuclei transcriptomics revealed that Lexis regulates a distinct population of thermogenic adipocytes. We systematically map Lexis motif preferences and show that it regulates the thermogenic program through the activity of the metabolic GWAS gene and WNT modulator TCF7L2. Collectively, our studies uncover a new mode of crosstalk between PPARγ and WNT signaling that preserves white adipose tissue plasticity.
2023-09-27 | GSE216272 | GEO
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
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 | GSE245480 | GEO
Project description:Interplay between parenchymal energy-storing white adipose cells and thermogenic beige adipocytes contributes to obesity and insulin resistance. Irrespective of cellular origin or specialized niche, adipocytes require the activity of the nuclear receptor peroxisome proliferator activated receptor gamma (PPARγ) for proper function. Exposure to cold or adrenergic signaling enriches thermogenic cells though multiple pathways that act synergistically with PPARγ, however, the molecular mechanisms by which PPARγ licenses white adipose tissue (WAT) to preferentially adopt a thermogenic or white adipose fate in response to dietary cues or thermoneutral conditions are not fully elucidated. Here, we show that a PPARγ-long noncoding RNA (lncRNA) axis integrates canonical and noncanonical thermogenesis to restrain white adipose tissue heat dissipation during thermoneutrality and diet-induced obesity (DIO). Pharmacologic inhibition or genetic deletion of the lncRNA Lexis, enhances UCP-1 dependent and independent thermogenesis. Adipose tissue specific deletion of Lexis counteracted diet-induced obesity, improved insulin sensitivity, and enhanced energy expenditure. Single-nuclei transcriptomics revealed that Lexis regulates a distinct population of thermogenic adipocytes. We systematically map Lexis motif preferences and show that it regulates the thermogenic program through the activity of the metabolic GWAS gene and WNT modulator TCF7L2. Collectively, our studies uncover a new mode of crosstalk between PPARγ and WNT signaling that preserves white adipose tissue plasticity.
2023-09-27 | GSE216608 | GEO
Project description:The change in ambient temperature is one of the risk factors for the aggravation of bronchial asthma (BA). Yet, whether the ambient temperature influences the immune functions associated with allergic asthma remains unknown. In this study, we treated asthmatic mice with standard temperature (ST, 20 °C) or thermoneutral temperature (TT, 30 °C). The results showed that the airway inflammatory cell counts in bronchoalveolar lavage fluid (BALF) and airway hyperresponsiveness (AHR) were significantly reduced in the mice treated with TT as compared with the mice treated with ST. The imbalance of Th1/Th2 response in the lung was improved following housing the mice at TT. In addition, the pulmonary Treg cells were increased in asthmatic mice after TT treatment. The temperature stress (29 °C and 41 °C) drove naïve CD4T cells towards Th2 cells. Our data demonstrate that the change of ambient temperature was a risk factor to aggravate experimental asthma.
| S-EPMC5540912 | biostudies-other