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Thermoneutral housing regulates intestinal tissue tolerance

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE158488 | GEO | 2020/09/25

REPOSITORIES: GEO

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Thermoneutral housing regulates intestinal tissue tolerance

Project description:Thermoneutral housing regulates intestinal tissue tolerance

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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.

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A PPARγ-lncRNA axis modulates thermoneutral remodeling of white adipose tissue

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.

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A PPARγ-lncRNA axis modulates thermoneutral remodeling of white adipose tissue [snRNA-seq]

2023-09-27 | GSE216608 | GEO

RNA-sequencing of inguinal adipose tissue from wild type and adipocyte specific HIF2a knock-out mice upon thermoneutral and cold exposure

Project description:Adipose tissue plays an important role in the regulation of wholebody energy homeostasis, depending on external environments. Upon cold acclimation, brown and beige adipocytes dissipate mitochondrial proton gradient generating heat via uncoupling protein 1. Due to increasing demands for oxygen during thermogenesis, adipose tissue could become hypoxic upon cold exposure. Hypoxia-inducible factors (HIFs) are one of the major transcription factors which are involved in various cellular responses under hypoxic condition. Although HIFs regulate diverse metabolic processes with selective target gene expression, their roles in thermogenic adipocytes are still elusive. In this study, we demonstrate that adipocyte HIF2a regulate thermogenic activity upon cold stimuli. To investigate molecular mechanisms of adipocyte HIF2a upon thermoneutral and cold exposure, we report the transcriptomes of inguinal adipose tissue from WT and adipocyte specific HIF2a knock-out mice.

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Project description:A thermogenic fat-epithelium cell axis regulates intestinal tissue tolerance

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Enterobacter ludwigii protects DSS-induced colitis through choline-mediated immune tolerance

Project description:Commensal intestinal bacteria play key roles in regulating cells mediating immune tolerance; however, bacterial strains and related metabolites directly involved in this regulation are largely unknown. Here, using a mouse model of dextran sulfate sodium (DSS)-induced colitis combined with different antibiotic treatment, Enterobacter ludwigii, abundant in microbiota of mice treated with metronidazole, was screened out to have prophylactic and therapeutic effects on DSS-induced colitis with or without the presence of complex intestinal bacteria. E. ludwigii was demonstrated to induce CD103+DC and Treg-mediated immune tolerance for colitis remission using in vitro and in vivo experiments. Moreover, choline, one of E. ludwigii metabolites, was identified to increase DCs’ immune tolerance to promote Treg differentiation. E. ludwigii was found to induce DCs’ immune tolerance ability for Treg differentiation through choline and α7nAChR-mediated RA and TGF-β upregulation, resulting in protecting mice against DSS-induced colitis. This study provides potential therapeutic approaches for IBD.

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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

Molecular characterization of supraclavicular and subcutaneous abdominal adipose tissue samples collected during CE (cold exposure) and TN (thermoneutral) conditions

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2016-05-26 | E-MTAB-4031 | biostudies-arrayexpress

Effect of deletion of carnitine palmitoyltransferase2 on interscapular BAT gene expression upon adrenergic stimulation in thermoneutral acclimatized mice

Project description:Ambient temperature affects energy intake and expenditure to maintain homeostasis in a continuously fluctuating environment. Here, mice with an adipose-specific defect in fatty acid oxidation (Cpt2A-/-) were subjected to varying temperature to determine the role of adipose bioenergetics to environmental adaptation. Cpt2A-/- brown adipose tissue (BAT) failed to induce thermogenic genes such as Ucp1 and Pgc1Î± in response to adrenergic stimulation, which is exacerbated by increasing temperature. Thermoneutrality induced a mitochondrial DNA stress in Cpt2A-/- BAT that resulted in a loss of classical interscapular BAT, but did not affect body weight gain or glucose tolerance in response to a high-fat diet. In this dataset, we include the expression data obtained from dissected mouse interscapular brown adipose tissue from mice acclimatized to thermoneutrality (30C) with and without beta3adrenergic stimulation with and without the deletion of carnitine palmitoyltransferase 2 (i.e., adipose unable to beta-oxidize long chain fatty acids in mitochondria). WildType and Cpt2A KnockOut mice were treated either with or without beta3adrenergic stimulation, thus four classes. Three biologic replicates were compared per class, thus twelve mice.

2016-02-04 | E-GEOD-72210 | biostudies-arrayexpress

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