Letters to the Editor |
The Department of Pharmacology, Therapeutics, and Toxicology, Wales Heart Research Institute, Cardiff University, Wales College of Medicine, Cardiff, United Kingdom
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
To the Editor:
With interest we read the recent report by Bisoendial et al in Circulation Research regarding their observation that infusion of C reactive protein (CRP) into humans induces the release of inflammatory mediators and coagulation factors.1 The CRP used in this study was generated in Escherichia coli, therefore there is a major possibility of the CRP being contaminated with bacterial products. Although the authors tried to remove endotoxin contamination using gel-filtration, in our opinion this is not a very rigorous method. The kinetics of Bisoendial et al observations suggests that endotoxin contamination and not CRP itself is responsible for their observations. This is especially clear considering the levels of CRP found in the plasma and the kinetics of IL-6 and IL-8 induction. The authors observe a continuous presence of CRP, which even increases after 24 hours, most likely attributable to the generation of CRP in the volunteer. If, as the authors suggest, their observation is caused by CRP itself, this would suggest that CRP can directly or indirectly increase its own synthesis; this would be a self-perpetuating effect and CRP levels would keep increasing until maximal achievable levels were obtained. However, IL-6 and IL-8 levels peak after 4 hours and are back to baseline levels at 8 hours. If CRP were responsible for the increased expression of these cytokines, levels would not peak, but because of the continuous and increasing levels of CRP, IL-6, and IL-8 levels would keep increasing similar to CRP. The kinetics of the
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R. Bisoendial, J. Kastelein, and E. Stroes Letter to the Editor: In response to van den Berg et al: Circ. Res., September 30, 2005; 97(7): e71 - e71. [Full Text] [PDF] |
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