Publications by authors named "Chris J Kuckleburg"

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).
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During sepsis, endothelial cells are both a source and target of pro-inflammatory cytokines (e.g. IL-1alpha, IL-1beta, TNFalpha and others), which may be detrimental to vascular homeostasis.

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Exposure of endothelial cells to lipid A-containing molecules, such as lipopolysaccharide (LPS) or lipooligosaccharide (LOS), causes the release of purinergic compounds [e.g., adenosine 5'-triphosphate (ATP)] and can lead to apoptosis.

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Vasculitis is commonly seen during systemic Haemophilus somnus infections. Although, the mechanism of vascular damage is not completely understood, in a previous report we demonstrated that H. somnus and its lipooligosaccharide (LOS) induced apoptosis in bovine pulmonary artery endothelial cells in vitro.

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