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Tumor necrosis factor-alpha enhances Haemophilus somnus lipooligosaccharide-induced apoptosis of bovine endothelial cells
Authors:Sylte Matt J  Kuckleburg Chris J  Leite Fabio P  Inzana Thomas J  Czuprynski Charles J
Institution:

aDepartment of Pathobiological Sciences, University of Wisconsin, 4174 Veterinary Medicine Building, 2015 Linden Dr., Madison, WI 53706, USA

bCenter for Molecular Medicine and Infectious Diseases, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061-0342, USA

Abstract:Haemophilus somnus lipooligosaccharide (LOS)-induced apoptosis of bovine pulmonary artery endothelial cells has been shown previously to be dependent on capsase-8 activation. Activation of caspase-8 can occur via a death receptor-dependent mechanism (e.g., TNF-greek small letter alpha binding to TNF-greek small letter alpha receptor 1 (TNF-R1)). In this study, we tested the hypothesis that TNF-greek small letter alpha can enhance LOS-induced apoptosis of bovine endothelial cells. Addition of exogenous recombinant human TNF-greek small letter 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-greek small letter alpha, LOS or TNF-greek small letter 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.
Keywords:Tumor necrosis factor-alpha  Endothelial cell  Apoptosis  Lipooligosaccharide  Haemophilus somnus
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