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Short-term hyperoxia does not exert immunologic effects during experimental murine and human endotoxemia.

Kiers D, Gerretsen J, Janssen E, John A, Groeneveld R, van der Hoeven JG, Scheffer GJ, Pickkers P, Kox M - Sci Rep (2015)

Bottom Line: 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.Our results indicate that hyperoxia does not exert direct anti-inflammatory effects and temper expectations of using it as an immunomodulatory treatment strategy.

View Article: PubMed Central - PubMed

Affiliation: Department of Intensive Care Medicine, Radboud university medical center, Geert Grooteplein Zuid 10, Nijmegen, 6500 HB, Netherlands.

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.

No MeSH data available.


Related in: MedlinePlus

Cytokine concentrations in different compartments in mice.Plasma, spleen, liver, and lung concentrations of (a)TNF-α, (b) IL-6, (c) KC, and (d) IL-10150 minutes after normoxia/hyperoxia (90 minutesafter LPS/placebo administration). Concentrations are represented asmean ± SEM. *indicatesp < 0.05.
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f1: Cytokine concentrations in different compartments in mice.Plasma, spleen, liver, and lung concentrations of (a)TNF-α, (b) IL-6, (c) KC, and (d) IL-10150 minutes after normoxia/hyperoxia (90 minutesafter LPS/placebo administration). Concentrations are represented asmean ± SEM. *indicatesp < 0.05.

Mentions: Hyperoxia was well tolerated and did not increase cytokine levels in plasma ortissue homogenates in placebo-treated mice (Fig. 1). LPSadministration resulted in increased cytokine levels in tissue homogenates, withthe exception of IL-6 in liver, and IL-10 in spleen, liver, and lunghomogenates. Apart from a slight, but statistically significant, reduction inplasma KC, hyperoxia did not affect LPS-induced cytokine concentrations.


Short-term hyperoxia does not exert immunologic effects during experimental murine and human endotoxemia.

Kiers D, Gerretsen J, Janssen E, John A, Groeneveld R, van der Hoeven JG, Scheffer GJ, Pickkers P, Kox M - Sci Rep (2015)

Cytokine concentrations in different compartments in mice.Plasma, spleen, liver, and lung concentrations of (a)TNF-α, (b) IL-6, (c) KC, and (d) IL-10150 minutes after normoxia/hyperoxia (90 minutesafter LPS/placebo administration). Concentrations are represented asmean ± SEM. *indicatesp < 0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4663498&req=5

f1: Cytokine concentrations in different compartments in mice.Plasma, spleen, liver, and lung concentrations of (a)TNF-α, (b) IL-6, (c) KC, and (d) IL-10150 minutes after normoxia/hyperoxia (90 minutesafter LPS/placebo administration). Concentrations are represented asmean ± SEM. *indicatesp < 0.05.
Mentions: Hyperoxia was well tolerated and did not increase cytokine levels in plasma ortissue homogenates in placebo-treated mice (Fig. 1). LPSadministration resulted in increased cytokine levels in tissue homogenates, withthe exception of IL-6 in liver, and IL-10 in spleen, liver, and lunghomogenates. Apart from a slight, but statistically significant, reduction inplasma KC, hyperoxia did not affect LPS-induced cytokine concentrations.

Bottom Line: 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.Our results indicate that hyperoxia does not exert direct anti-inflammatory effects and temper expectations of using it as an immunomodulatory treatment strategy.

View Article: PubMed Central - PubMed

Affiliation: Department of Intensive Care Medicine, Radboud university medical center, Geert Grooteplein Zuid 10, Nijmegen, 6500 HB, Netherlands.

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.

No MeSH data available.


Related in: MedlinePlus