Abstract
The maintenance of oxygen homeostasis in human tissues is mediated by several cellular adaptations in response to low-oxygen stress, called hypoxia. A decrease in tissue oxygen levels is initially counteracted by increasing local blood flow to overcome diminished oxygenation and avoid hypoxic stress. However, studies have shown that the physiological oxygen concentrations in several tissues are much lower than atmospheric (normoxic) conditions, and the oxygen supply is finely regulated in individual cell types. The gastrointestinal tract has been described to subsist in a state of physiologically low oxygen level and is thus depicted as a tissue in the state of constant low-grade inflammation. The intestinal epithelial cell layer plays a vital role in the immune response to inflammation and infections that occur within the intestinal tissue and is involved in many of the adaptation responses to hypoxic stress. This is especially relevant in the context of inflammatory disorders, such as inflammatory bowel disease (IBD). Therefore, this review aims to describe the intestinal epithelial cellular response to hypoxia and the consequences for host interactions with invading gastrointestinal bacterial pathogens.
Highlights
The maintenance of oxygen homeostasis in human tissues is mediated by several cellular adaptations in response to low-oxygen stress, called hypoxia
Hypoxia during infections and inflammation Hypoxic stress, that occurs when cellular oxygen demand is higher than its supply, is a commonplace in tissues faced with infection and inflammation [7, 8]
There are many factors that result in this oxygen deficit, including the demands of innate immune cells, such as neutrophils and macrophages that are recruited to the site of infection as well as those of invading pathogens that consume oxygen [9, 10]
Summary
The maintenance of oxygen homeostasis in human tissues is mediated by several cellular adaptations in response to low-oxygen stress, called hypoxia. These increased oxygen demands, in addition to the requirements of the resident cells of the infected tissue, can cause a severe drop in available oxygen levels, resulting in a state of hypoxia.
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