Hyperbaric oxygen inhibits stimulus-induced proinflammatory cytokine synthesis by human blood-derived monocyte-macrophages

Clin Exp Immunol. 2003 Oct;134(1):57-62. doi: 10.1046/j.1365-2249.2003.02248.x.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Cells, Cultured
  • Cytokines / immunology*
  • Humans
  • Hyperbaric Oxygenation*
  • Immunosuppression Therapy
  • Interleukin-1 / biosynthesis
  • Interleukin-1 / genetics
  • Lipid A / pharmacology
  • Lipopolysaccharides / pharmacology
  • Macrophages / immunology*
  • Phytohemagglutinins / pharmacology
  • RNA, Messenger / analysis
  • Stimulation, Chemical
  • Time Factors
  • Tumor Necrosis Factor-alpha / biosynthesis


  • Cytokines
  • Interleukin-1
  • Lipid A
  • Lipopolysaccharides
  • Phytohemagglutinins
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha