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Salmonella infection accelerates potential maturation of the intestinal epithelium

ABSTRACT: Salmonella infection accelerates potential maturation of the intestinal epithelium

PROVIDER: PRJNA1167207 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30840019.fastq.gz	Fastqsanger.gz
	SRR30840020.fastq.gz	Fastqsanger.gz
	SRR30840021.fastq.gz	Fastqsanger.gz
	SRR30840022.fastq.gz	Fastqsanger.gz
	SRR30840023.fastq.gz	Fastqsanger.gz

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Salmonella infection accelerates potential maturation of the intestinal epithelium

Project description:Postnatal establishment of enteric metabolic, host-microbial and immune homeostasis is the result of precisely timed and tightly regulated developmental and adaptive processes. Here, we show that infection with the invasive enteropathogen Salmonella Typhimurium results in a Myd88-dependent accelerated maturation of the neonatal epithelium with premature appearance of antimicrobial, metabolic, developmental, and regenerative features of the adult tissue.

2024-12-17 | GSE278410 | GEO

Acetate increases the maturation of the preterm intestinal epithelium

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Targeting CFTR and FGF2 and TGFβ1 Pathways with MSC-Derived Extracellular Vesicles to Promote Functional Maturation of Preterm Intestinal Epithelium

Project description:Preterm birth disrupts the critical maturation of the intestinal epithelium, leading to compromised digestive and absorptive functions. This study explores the potential of mesenchymal stem cell (MSC)-derived extracellular vesicles (EVs) to promote the maturation of human preterm intestinal epithelial cells. By establishing human preterm intestinal organoids derived from the ileal tissue of a neonate born at 27 weeks gestational age, we demonstrate that treatment with EVs, particularly the EV39 line, significantly enhances the expression of adult-type enterocyte markers, including genes involved in lipid and nutrient transport, digestive enzymes, and epithelial barrier integrity. These maturation signatures were identified through reanalysis of multiple single-cell RNA sequencing (scRNA-seq) datasets, revealing distinct enterocyte differentiation trajectories and key maturation-specific gene expression profiles. Notably, these maturation effects were dependent on cystic fibrosis transmembrane conductance regulator (CFTR) activity, as CFTR inhibition reversed the observed benefits. Proteomic analysis identified FGF2 and TGFβ1 as key ligands mediating the effects of EV39. Co-treatment with FGF2 and TGFβ1 further enhanced epithelial barrier integrity and fatty acid uptake, highlighting the translational potential of EV39 or its ligands in promoting intestinal functional maturation in preterm infants.

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Culturing C2C12 myotubes on micromolded gelatin hydrogels accelerates myotube maturation

Project description:Culturing C2C12 myotubes on micromolded gelatin hydrogels accelerates myotube maturation

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Thyroid hormone augmentation accelerates hair cell maturation in human cochlear organoids

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Transcriptional and epigenomic profiling identifies YAP signaling as a key regulator of intestinal epithelium maturation

Project description:Transcriptional and epigenomic profiling identifies YAP signaling as a key regulator of intestinal epithelium maturation

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Early life antibiotics influence in vivo and in vitro mouse intestinal epithelium maturation and functioning

Project description:Early life antibiotics influence in vivo and in vitro mouse intestinal epithelium maturation and functioning

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The Ets domain transcription factor Spdef drives maturation of Goblet and Paneth cells in the intestinal epithelium

Project description:BACKGROUND & AIMS: Stems cells within the intestinal epithelium generate daughter cells which undergo lineage commitment and maturation through the concerted action of the Wnt and Notch signalling cascades. Both pathways, in turn, regulate transcription factor networks which further define differentiation towards either enterocytes or one of three secretory cell lineages (Paneth, goblet or enteroendocrine cells). In this manuscript, we identified the Ets domain transcription factor, Spdef, as a novel lineage maker of goblet and Paneth cells. METHODS: To address the function of Spdef in vivo, we inactivated the Spdef gene and analysed the intestinal phenotype using a range of histological techniques and DNA microarray profiling. RESULTS: In accordance with the expression data we found that loss of Spdef severely impaired the maturation of goblet and Paneth cells and conversely lead to an accumulation of immature secretory progenitors. Moreover, we provide evidence suggesting that Spdef positively and negatively regulates a specific subset of goblet and Paneth cell genes including Cryptdins, Mmp7, Ang4, Kallikreins, and Muc2. CONCLUSION: We propose a model whereby Spdef acts downstream of Math1 to promote terminal differentiation of a secretory progenitor pool towards Paneth and goblet cells. Keywords: expression profiling

2010-02-10 | GSE14892 | GEO

Smoking accelerated aging of the small airway epithelium

Project description:Aging involves multiple biologically complex processes characterized by a decline in cellular homeostasis over time leading to a loss and impairment of physiological integrity and function. Specific cellular hallmarks of aging include abnormal gene expression patterns, shortened telomeres and associated biological dysfunction. Like all organs, the lung demonstrates both physiological and structural changes with age that result in a progressive decrease in lung function in healthy individuals. Cigarette smoking accelerates lung function decline over time, suggesting smoking accelerates aging of the lung. Based on this data, we hypothesized that cigarette smoking accelerates the aging of the small airway epithelium, the cells that take the initial brunt of inhaled toxins from the cigarette smoke and one of the primary sites of pathology associated with cigarette smoking. Using the sensitive molecular parameters of aging-related gene expression and telomere length, the aging process of the small airway epithelium was assessed in age matched healthy nonsmokers and healthy smokers with no physical manifestation of lung disease or abnormalities in lung function. Analysis of a 73 gene aging signature demonstrated that smoking significantly dysregulates 18 aging-related genes in the small airway epithelium. In an independent cohort of male subjects, smoking significantly reduced telomere length in the small airway epithelium of smokers by 14% compared to nonsmokers. These data provide biologic evidence that prior to the clinical manifestation of lung disease; smoking accelerates aging of the small airway epithelium.

2015-08-17 | GSE52237 | GEO

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