
Exposure to hyperbaric oxygen induces tumour necrosis factor‐alpha (TNF‐α) secretion from rat macrophages
Author(s) -
LAHAT N.,
BITTERMAN H.,
YANIV N.,
KINARTY A.,
BITTERMAN N.
Publication year - 1995
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1995.tb03867.x
Subject(s) - tumor necrosis factor alpha , secretion , immunology , necrosis , macrophage , tumor necrosis factor α , hyperbaric oxygen , alpha (finance) , medicine , biology , pathology , endocrinology , in vitro , biochemistry , anesthesia , construct validity , nursing , patient satisfaction
SUMMARY We investigated the secretion of TNF‐α by monocytes and macrophages derived from the peripheral blood, spleen, and lungs after a single exposure to a therapeutic profile of hyperbaric oxygen (HBO). Rats were exposed for 90 min to either 100% oxygen at 0 28 MPa (2–8 atmospheres absolute) or air. Immediately after exposure, mononuclear cells were isolated from blood, spleen, and lungs and cultured for 18h. The secretion of TNF‐α from the cultured monocytes/macrophages was determined with and without stimulation with lipopolysaccharide (LPS). Exposure to hyperbaric oxygen induced a significant increase in the spontaneous ex vivo secretion of TNF‐α (without LPS) by mononuclear cells from the blood, spleen, and lung (P < 0 05 from air controls). Stimulation with LPS after exposure to HBO induced a significant increase in TNF‐α secretion by lung and spleen macrophages compared with air controls (P<005). However, absolute TNF‐α levels were not significantly higher than those achieved ‘spontaneously’ in macrophages exposed to HBO without LPS. Stimulation with LPS induced a marked increase in secretion of TNF‐α from blood monocytes after exposure to air, but not after exposure to HBO. These results provide evidence in support of a role played by TNF‐α in mediating HBO effects on different tissues and their immune responses.