EXPOSURE TO HYPERBARIC-OXYGEN INDUCES TUMOR-NECROSIS-FACTOR-ALPHA (TNF-ALPHA) SECRETION FROM RAT MACROPHAGES

Citation
N. Lahat et al., EXPOSURE TO HYPERBARIC-OXYGEN INDUCES TUMOR-NECROSIS-FACTOR-ALPHA (TNF-ALPHA) SECRETION FROM RAT MACROPHAGES, Clinical and experimental immunology, 102(3), 1995, pp. 655-659
Citations number
34
Categorie Soggetti
Immunology
ISSN journal
00099104
Volume
102
Issue
3
Year of publication
1995
Pages
655 - 659
Database
ISI
SICI code
0009-9104(1995)102:3<655:ETHIT(>2.0.ZU;2-J
Abstract
We investigated the secretion of TNF-alpha by monocytes and macrophage s derived from the peripheral blood, spleen, and lungs after a single exposure to a therapeutic profile of hyperbaric oxygen (HBO). Rats wer e exposed for 90 min to either 100% oxygen at 0.28 MPa (2.8 atmosphere s absolute) or air. Immediately after exposure, mononuclear cells were isolated from blood, spleen, and lungs and cultured for 18 h. The sec retion of TNF-alpha from the cultured monocytes/macrophages was determ ined with and without stimulation with lipopolysaccharide (LPS). Expos ure to hyperbaric oxygen induced a significant increase in the spontan eous ex vivo secretion of TNF-alpha (without LPS) by mononuclear cells from the blood, spleen, and lung (P < 0.05 from air controls). Stimul ation with LPS after exposure to HBO induced a significant increase in TNF-alpha secretion by lung and spleen macrophages compared with air controls (P < 005). However, absolute TNF-alpha levels were not signif icantly higher than those achieved 'spontaneously' in macrophages expo sed to HBO without LPS. Stimulation with LPS induced a marked increase in secretion of TNF-alpha from blood monocytes after exposure to air, but not after exposure to HBO. These results provide evidence in supp ort of a role played by TNF-alpha in mediating HBO effects on differen t tissues and their immune responses.