title: Hyperbaric oxygen inhibits stimulus-induced proinflammatory cytokine synthesis by human blood-derived monocyte-macrophages.
abstract: 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 degrees 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-1beta synthesized in response to lipopolysaccharide by 23%, lipid A by 45%, phytohaemagglutinin A (PHA) by 68%, and tumour necrosis factor (TNF)-alpha by 27%. HBO suppressed lipopolysaccharide-, lipid A- and PHA-induced TNF-alpha by 29%, 31% and 62%, respectively. HBO transiently reduced PHA-induced steady state IL-1beta 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-1beta than cells cultured under control conditions. In summary, HBO exposure transiently suppresses stimulus-induced proinflammatory cytokine production and steady state RNA levels.
authors.affiliation: Baystate Medical Center, Tufts University School of Medicine, Springfield, MA 01199, USA.
authors.forename: R M
authors.initials: RM
authors.lastname: Benson
authors.forename: L M
authors.initials: LM
authors.lastname: Minter
authors.forename: B A
authors.initials: BA
authors.lastname: Osborne
authors.forename: E V
authors.initials: EV
authors.lastname: Granowitz
mesh_terms: D002478:Cells, Cultured; D016207:Cytokines / Q000276:immunology*; D006801:Humans; D006931:Hyperbaric Oxygenation; D007165:Immunosuppression Therapy; D007375:Interleukin-1 / Q000096:biosynthesis / Q000235:genetics; D008050:Lipid A / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000494:pharmacology; D008264:Macrophages / Q000276:immunology*; D010835:Phytohemagglutinins / Q000494:pharmacology; D012333:RNA, Messenger / Q000032:analysis; D013268:Stimulation, Chemical; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D016207:Cytokines; D007375:Interleukin-1; D008050:Lipid A; D008070:Lipopolysaccharides; D010835:Phytohemagglutinins; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha