E Wolfson
6 Papers
178 Citations
E Wolfson is an academic researcher. The author has contributed to research in topics: Lipopolysaccharide & Tumor necrosis factor alpha. The author has an hindex of 6, co-authored 6 publications.
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Papers
Adaptation to bacterial lipopolysaccharide controls lipopolysaccharide-induced tumor necrosis factor production in rabbit macrophages.
TL;DR: Treatment of elicited peritoneal exudate rabbit macrophages with two doses of LPS given 9 h apart results in a marked reduction in TNF production by the second LPS exposure, providing an explanation for the observation that two intravenous injections of lipopolysaccharide spaced 5 h apart in rabbits cause tumor necrosis factor/cachectin levels to rise in the blood only after the first LPS injection.
Lipopolysaccharide (LPS) recognition in macrophages. Participation of LPS-binding protein and CD14 in LPS-induced adaptation in rabbit peritoneal exudate macrophages.
TL;DR: Results show that complexes of LPS and LBP are more effective than LPS alone in inducing adaptation to LPS, and LPS-induced hyporesponsiveness probably results from changes in cellular elements distinct from CD14 that are involved in either LPS recognition or L PS-specific signal transduction.
Regulatory mechanisms of host responsiveness to endotoxin (lipopolysaccharide).
TL;DR: In this article, the authors discuss regulation of LPS-M phi interactions by LPS binding plasma proteins and by changes in M phi responsiveness to lipopolysaccharide (LPS).
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Tumour necrosis factor alpha antibody protects against lethal meningococcaemia.
TL;DR: The results indicate that TNF‐α has a deleterious effect in this model of bacteraemia, and identification of the critical factors that determine the action of T NF‐α during lethal bacterAemia will lead to a better understanding of these diseases and the development of appropriate therapeutic intervention.
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Participation of tumor necrosis factor in the mediation of gram negative bacterial lipopolysaccharide-induced injury in rabbits.
TL;DR: Evidence is provided that prior infusion of anti-TNF antibody resulted in neutralization of the LPS-induced serum TNF activity and provided significant protection from the development of hypotension, fibrin deposition, and lethality.