AI Article Synopsis
- Previous research indicated that the apoptosis of bovine pulmonary artery endothelial cells caused by Haemophilus somnus lipooligosaccharide (LOS) relies on the activation of caspase-8.
- This study aimed to determine if TNF-alpha could enhance this apoptosis; however, while TNF-alpha alone did not induce or enhance apoptosis, blocking protein synthesis with cycloheximide significantly increased apoptosis when combined with TNF-alpha or LOS.
- Ultimately, the results suggest that LOS-induced apoptosis is partially mediated by a death pathway involving TNF-alpha receptor 1 (TNF-R1).
Article Abstract
Haemophilus somnus lipooligosaccharide (LOS)-induced apoptosis of bovine pulmonary artery endothelial cells has been shown previously to be dependent on caspase-8 activation. Activation of caspase-8 can occur via a death receptor-dependent mechanism (e.g., TNF-alpha binding to TNF-alpha receptor 1 (TNF-R1)). In this study, we tested the hypothesis that TNF-alpha can enhance LOS-induced apoptosis of bovine endothelial cells. Addition of exogenous recombinant human TNF-alpha alone failed to cause apoptosis, or enhance LOS-induced apoptosis, of bovine endothelial cells. However, blocking de novo protein synthesis by addition of cycloheximide significantly enhanced apoptosis of bovine endothelial cells by TNF-alpha, LOS or TNF-alpha and LOS in combination. Conversely, addition of soluble recombinant human (sTNF-R1) diminished LOS-induced apoptosis. Overall, these data suggest that LOS-mediated apoptosis may be due, in part, to activation of a TNR-R1-dependent death pathway.
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| http://dx.doi.org/10.1016/j.vetimm.2005.10.010 | DOI Listing |
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