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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

Circulating leukocytes in healthy volunteers.Numbers of circulating (a) neutrophils, (b) monocytes and(c) lymphocytes. The period that subjects were fitted with therespiratory helmet and breathed hyperoxic or normoxic air is indicated witha grey box. In the endotoxemia groups, LPS was administered atT = 0 hours. Data are expressed asmean ± SEM NORM-E: normoxic endotoxemia,HYPER-E: hyperoxic endotoxemia, HYPER: hyperoxia.
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f4: Circulating leukocytes in healthy volunteers.Numbers of circulating (a) neutrophils, (b) monocytes and(c) lymphocytes. The period that subjects were fitted with therespiratory helmet and breathed hyperoxic or normoxic air is indicated witha grey box. In the endotoxemia groups, LPS was administered atT = 0 hours. Data are expressed asmean ± SEM NORM-E: normoxic endotoxemia,HYPER-E: hyperoxic endotoxemia, HYPER: hyperoxia.

Mentions: Numbers of circulating neutrophils, monocytes, and lymphocytes changedsignificantly, but to no clinically relevant extent, over time in thehyperoxia group (Fig. 4). LPS administration typicallyresulted in neutrophilia, with transient lympho- and monocytopenia.Hyperoxia did not affect LPS-induced changes in any of the leukocytesubsets.


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)

Circulating leukocytes in healthy volunteers.Numbers of circulating (a) neutrophils, (b) monocytes and(c) lymphocytes. The period that subjects were fitted with therespiratory helmet and breathed hyperoxic or normoxic air is indicated witha grey box. In the endotoxemia groups, LPS was administered atT = 0 hours. Data are expressed asmean ± SEM NORM-E: normoxic endotoxemia,HYPER-E: hyperoxic endotoxemia, HYPER: hyperoxia.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f4: Circulating leukocytes in healthy volunteers.Numbers of circulating (a) neutrophils, (b) monocytes and(c) lymphocytes. The period that subjects were fitted with therespiratory helmet and breathed hyperoxic or normoxic air is indicated witha grey box. In the endotoxemia groups, LPS was administered atT = 0 hours. Data are expressed asmean ± SEM NORM-E: normoxic endotoxemia,HYPER-E: hyperoxic endotoxemia, HYPER: hyperoxia.
Mentions: Numbers of circulating neutrophils, monocytes, and lymphocytes changedsignificantly, but to no clinically relevant extent, over time in thehyperoxia group (Fig. 4). LPS administration typicallyresulted in neutrophilia, with transient lympho- and monocytopenia.Hyperoxia did not affect LPS-induced changes in any of the leukocytesubsets.

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