Abstract
Oxygen therapy to maintain tissue oxygenation is one of the cornerstones of critical care. Therefore, hyperoxia is often encountered in critically ill patients. Epidemiologic studies have demonstrated that hyperoxia may affect outcome, although mechanisms are unclear. Immunologic effects might be involved, as hyperoxia was shown to attenuate inflammation and organ damage in preclinical models. However, it remains unclear whether these observations can be ascribed to direct immunosuppressive effects of hyperoxia or to preserved tissue oxygenation. In contrast to these putative anti-inflammatory effects, hyperoxia may elicit an inflammatory response and organ damage in itself, known as oxygen toxicity. Here, we demonstrate that, in the absence of systemic inflammation, short-term hyperoxia (100% O2 for 2.5 hours in mice and 3.5 hours in humans) does not result in increased levels of inflammatory cytokines in both mice and healthy volunteers. Furthermore, we show that, compared with room air, hyperoxia does not affect the systemic inflammatory response elicited by administration of bacterial endotoxin in mice and man. Finally, neutrophil phagocytosis and ROS generation are unaffected by short-term hyperoxia. Our results indicate that hyperoxia does not exert direct anti-inflammatory effects and temper expectations of using it as an immunomodulatory treatment strategy.
Highlights
Hyperoxia, or resulted from preserved tissue oxygenation during severe hemodynamic instability, thereby preventing additional tissue damage and subsequent inflammation[13,14]
We demonstrate that short-term hyperoxia neither induces increased levels of cytokines in itself, nor modulates the cytokine response during systemic inflammation induced by endotoxin administration in mice and healthy volunteers
Both in the presence and absence of systemic inflammation in humans, no relevant effects of short-term hyperoxia were observed on temperature, flu-like symptoms, leukocyte counts, ex vivo whole blood cytokine production, neutrophil phagocytosis, and neutrophil reactive oxygen species (ROS) generation
Summary
Hyperoxia, or resulted from preserved tissue oxygenation during severe hemodynamic instability, thereby preventing additional tissue damage and subsequent inflammation[13,14]. If hyperoxia has intrinsic anti-inflammatory effects, it could be a promising treatment option in inflammatory conditions in the ICU, as oxygen is affordable and widely available. Evidence of direct immunologic effects of hyperoxia in animals and humans in vivo is lacking. We investigated the intrinsic immunologic effects of short-term hyperoxia in the presence and absence of systemic inflammation elicited by administration of LPS in mice and man, primarily reflected by circulating cytokine levels. As hyperoxia has been reported to impair leukocyte functions (e.g. cytokine production[7], phagocytosis and killing9), whole blood ex vivo cytokine production, neutrophil phagocytosis, and intracellular generation of reactive oxygen species (ROS) were assessed in humans
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