AI Article Synopsis
- The study examined how subthreshold hyperoxia and the inflammatory cytokine TNF-alpha affect ICAM-1 expression in bovine lung microvascular endothelial cells.
- Exposure to 50% hyperoxia alone did not alter ICAM-1 levels, indicating it's a subthreshold condition.
- However, when combined with low levels of TNF-alpha, total ICAM-1 expression increased by about 30% compared to normal conditions, and the release of soluble ICAM-1 into the culture medium also rose, suggesting a heightened response to inflammation under hyperoxic conditions.
Article Abstract
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.
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| http://dx.doi.org/10.3109/01902149709087367 | DOI Listing |
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Article Synopsis
- The study examined how subthreshold hyperoxia and the inflammatory cytokine TNF-alpha affect ICAM-1 expression in bovine lung microvascular endothelial cells.
- Exposure to 50% hyperoxia alone did not alter ICAM-1 levels, indicating it's a subthreshold condition.
- However, when combined with low levels of TNF-alpha, total ICAM-1 expression increased by about 30% compared to normal conditions, and the release of soluble ICAM-1 into the culture medium also rose, suggesting a heightened response to inflammation under hyperoxic conditions.
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