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Regulation of Oxygen Homeostasis at the Intestinal Epithelial Barrier Site

期刊

出版社

MDPI
DOI: 10.3390/ijms22179170

关键词

oxygen; mitochondria; hypoxia; microbiota; IBD

资金

  1. Public Scholarship, Development, Disability Fund of the Republic of Slovenia
  2. Slovenian Research Agency [P1-0207]
  3. European Union H2020 ERA project [667824-EXCELLtoINNOV]
  4. La Caixa Foundation [100010434, LCF/PR/HR19/52160005]

向作者/读者索取更多资源

The unique biology of the intestinal epithelial barrier is linked to low oxygen pressure and hypoxia-inducible factor-dependent signaling; communication between microbiota and the gut plays a crucial role in maintaining oxygen homeostasis and intestinal health.
The unique biology of the intestinal epithelial barrier is linked to a low baseline oxygen pressure (pO(2)), characterised by a high rate of metabolites circulating through the intestinal blood and the presence of a steep oxygen gradient across the epithelial surface. These characteristics require tight regulation of oxygen homeostasis, achieved in part by hypoxia-inducible factor (HIF)-dependent signalling. Furthermore, intestinal epithelial cells (IEC) possess metabolic identities that are reflected in changes in mitochondrial function. In recent years, it has become widely accepted that oxygen metabolism is key to homeostasis at the mucosae. In addition, the gut has a vast and diverse microbial population, the microbiota. Microbiome-gut communication represents a dynamic exchange of mediators produced by bacterial and intestinal metabolism. The microbiome contributes to the maintenance of the hypoxic environment, which is critical for nutrient absorption, intestinal barrier function, and innate and/or adaptive immune responses in the gastrointestinal tract. In this review, we focus on oxygen homeostasis at the epithelial barrier site, how it is regulated by hypoxia and the microbiome, and how oxygen homeostasis at the epithelium is regulated in health and disease.

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