Abstract
In vitro and animal studies have shown that hypoxia and hyperoxia influence the innate immune response. Therefore, hypoxia and hyperoxia could be cheap, non-pharmacological, non-invasive treatment modalities to modulate inflammatory conditions. Hypoxia has shown to exert pro-inflammatory effects, supposedly mediated by the transcription factor hypoxia inducible factor 1α (HIF1α), whereas hyperoxia is related to immune suppression. However, apart from direct effects of oxygen status adjustment on the immune response, other mechanisms such as a hypoxia-induced stress response might play a role in humans in vivo as well. Up till now, the interplay between oxygen status adjustment and the innate immune response in humans in vivo has not been investigated.
Highlights
In vitro and animal studies have shown that hypoxia and hyperoxia influence the innate immune response
Hypoxia has shown to exert pro-inflammatory effects, supposedly mediated by the transcription factor hypoxia inducible factor 1a (HIF1a), whereas hyperoxia is related to immune suppression
Apart from direct effects of oxygen status adjustment on the immune response, other mechanisms such as a hypoxia-induced stress response might play a role in humans in vivo as well
Summary
In vitro and animal studies have shown that hypoxia and hyperoxia influence the innate immune response. Hypoxia and hyperoxia could be cheap, non-pharmacological, non-invasive treatment modalities to modulate inflammatory conditions. Hypoxia has shown to exert pro-inflammatory effects, supposedly mediated by the transcription factor hypoxia inducible factor 1a (HIF1a), whereas hyperoxia is related to immune suppression. Apart from direct effects of oxygen status adjustment on the immune response, other mechanisms such as a hypoxia-induced stress response might play a role in humans in vivo as well. The interplay between oxygen status adjustment and the innate immune response in humans in vivo has not been investigated
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