Affiliation:
1. Department of Medicine, Baystate Medical Center, Tufts University School of Medicine, Springfield, MA
2. Department of Veterinary and Animal Sciences, University of Massachusetts, Amherst, MA
Abstract
SUMMARY
Hyperbaric oxygen (HBO) is 100% oxygen administered at elevated atmospheric pressure to patients with inflammatory diseases. We developed an in vitro model to investigate the effects of HBO on stimulus-induced proinflammatory cytokine transcription and translation. Human blood-derived monocyte-macrophages were stimulated before being transferred to an HBO chamber where they were incubated at 97·9% O2, 2·1% CO2, 2·4 atmospheres absolute, 37°C. Controls were maintained in the same warm room at normoxia at sea level, hyperoxia or increased pressure alone. A 90-min HBO exposure inhibited IL-1β synthesized in response to lipopolysaccharide by 23%, lipid A by 45%, phytohaemagglutinin A (PHA) by 68%, and tumour necrosis factor (TNF)-α by 27%. HBO suppressed lipopolysaccharide-, lipid A- and PHA-induced TNF-α by 29%, 31% and 62%, respectively. HBO transiently reduced PHA-induced steady state IL-1β mRNA levels. Hyperoxia alone and pressure alone did not affect cytokine production. The immunosuppressive effect of HBO was no longer evident in monocyte-macrophages exposed to HBO for more than 3 h. Interestingly, cells exposed to HBO for 12 h synthesized more IL-1β than cells cultured under control conditions. In summary, HBO exposure transiently suppresses stimulus-induced proinflammatory cytokine production and steady state RNA levels.
Publisher
Oxford University Press (OUP)
Subject
Immunology,Immunology and Allergy
Cited by
102 articles.
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