Subthreshold hyperoxia potentiates TNF-alpha-induced ICAM-1 expression on cultured pulmonary microvascular endothelial cells.
The effects of combined exposure to subthreshold hyperoxia and the inflammatory cytokine tumor necrosis factor alpha (TNF-alpha) on the expression of intercellular adhesion molecule-1 (ICAM-1) were examined in bovine lung microvascular endothelial cells (BLuEC). The expression of total ICAM-1 was not affected by 50% hyperoxia conditions alone, indicating that this level is subthreshold for BLuEC. In the presence of 5 ng/mL TNF-alpha, which has minimal influence on BLuEC alone, the amount of total ICAM-1 expression under 50% hyperoxia was higher than that in normoxic conditions (approximately 30%) throughout the culture period. The amount of soluble ICAM-1 that has been released into the culture medium increased after joint exposure to hyperoxia and TNF-alpha. These results suggest that exposure to subthreshold hyperoxia, which does not by itself cause damage to the endothelial cells or induce ICAM-1 expression, potentiates the effects of low-level TNF-alpha exposure.
Kiguchi
T
T
5th Department of Internal Medicine, Tokyo Medical College, Ibaraki, Japan.
Takahashi
K
K
Uwabe
Y
Y
Nakamura
H
H
Kashiwabara
K
K
Yagyu
H
H
Matsuoka
T
T
D000818:Animals; D002417:Cattle; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000187:drug effects / Q000293:injuries / Q000378:metabolism; D018496:Hyperoxia / Q000378:metabolism*; D007249:Inflammation / Q000209:etiology / Q000378:metabolism; D018836:Inflammation Mediators / Q000633:toxicity; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008168:Lung / Q000187:drug effects* / Q000378:metabolism*; D055370:Lung Injury; D012995:Solubility; D014409:Tumor Necrosis Factor-alpha / Q000008:administration & dosage / Q000633:toxicity*
D018836:Inflammation Mediators; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D007770:L-Lactate Dehydrogenase