Abstract
Systemic inflammation is a pathogenetic component in a vast number of acute and chronic diseases such as sepsis, trauma, type 2 diabetes, atherosclerosis, and Alzheimers disease, all of which are associated with a substantial morbidity and mortality. However, the molecular mechanisms and physiological significance of the systemic inflammatory response are still not fully understood. The human endotoxin model, an in vivo model of systemic inflammation in which lipopolysaccharide is injected or infused intravenously in healthy volunteers, may be helpful in unravelling these issues. The present review addresses the basic changes that occur in this model. The activation of inflammatory cascades as well as organ-specific haemodynamic and functional changes after lipopolysaccharide are described, and the limitations of human-experimental models for the study of clinical disease are discussed. Finally, we outline the ethical considerations that apply to the use of human endotoxin model.
Keywords: Cytokine, diabetes, endotoxin, inflammation, LPS, interleukin-6, sepsis, tumor necrosis factor-α
Current Medicinal Chemistry
Title: Human Endotoxemia as a Model of Systemic Inflammation
Volume: 15 Issue: 17
Author(s): A. S. Andreasen, K. S. Krabbe, R. Krogh-Madsen, S. Taudorf, B. K. Pedersen and K. Moller
Affiliation:
Keywords: Cytokine, diabetes, endotoxin, inflammation, LPS, interleukin-6, sepsis, tumor necrosis factor-α
Abstract: Systemic inflammation is a pathogenetic component in a vast number of acute and chronic diseases such as sepsis, trauma, type 2 diabetes, atherosclerosis, and Alzheimers disease, all of which are associated with a substantial morbidity and mortality. However, the molecular mechanisms and physiological significance of the systemic inflammatory response are still not fully understood. The human endotoxin model, an in vivo model of systemic inflammation in which lipopolysaccharide is injected or infused intravenously in healthy volunteers, may be helpful in unravelling these issues. The present review addresses the basic changes that occur in this model. The activation of inflammatory cascades as well as organ-specific haemodynamic and functional changes after lipopolysaccharide are described, and the limitations of human-experimental models for the study of clinical disease are discussed. Finally, we outline the ethical considerations that apply to the use of human endotoxin model.
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Cite this article as:
Andreasen S. A., Krabbe S. K., Krogh-Madsen R., Taudorf S., Pedersen K. B. and Moller K., Human Endotoxemia as a Model of Systemic Inflammation, Current Medicinal Chemistry 2008; 15 (17) . https://dx.doi.org/10.2174/092986708784872393
DOI https://dx.doi.org/10.2174/092986708784872393 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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