There are many markers of endothelial activation and damage (sVCAM-1, von Wilebrand factor, D-dimer, etc. etc. etc.), and I need to decide for one (ideally) or two to measure in human blood that can tell me if the endothlium has been activated, damaged or dead. We want to look for indicators of activation of any vascularity that can have impact at a systemic level, to the point of possibly participating in septic shock or acute respiratory inflammatory syndrome, empyema, lung edema, deep vein thrombosis, etc (any poor outcome related with inflammation). The patiens will be mainly critical or hospital-bound, with respiratory symptoms, mainly related with infectious diseases. I will thank any ideas.
There is some variation in what marker is most appropriate, dependent upon the vascular endothelial type you are wanting to assess, e.g. pulmonary capillary, aortic..etc. If you can be more specific about your research question, I may be able to make some suggestions.
Thanks Chalotte. Indeed I was too general. We want to look for indicators of activation of any vascularity that can have impact at a systemic level, to the point of participating in septic shock or acute respiratory inflammatory syndrome, empyema, lung edema, deep vein thrombosis, etc (any poor outcome related with inflammation). The patiens will be mainly critical or hospital-bound, with respiratory symptoms, mainly related with infectious diseases. Thats the most specific I can get.
Still not clear. Is this in patients? You want to see whether NO is liberated or what? Leukocyte adherence, mediator release, expression of selectines, Shading of glycocalix??
I thought that you have to measure in vitro a free and bound thrombin and factor Xa.
Dr Meddahi Sadia
IMHO, among the easily measured plasma soluble markers quite sensitive are von Willebrand factor antigen (especially its large multimeric form) ans ICAM-1.
Soluble ICAM-1 is the best marker for endothelial damage (R&D Enzyme immuno assay).
I am agree with Thomas and Jacek. In your conditions, the best marker of endothelial activation is soluble ICAM-1.
In my opinion with (only) 2 factors to pick from I would go for VWF antigen detection since it is the marker for the ndex of endothelial dysfunction and further add s-ICAM since VWF has quite a big variance (depends also on the power of your study)
For additional markers you could decide to also look in to e-Selectin levels, circulating endothelial cells or maybe even thrombin generation time and microparticles.
I recently read this paper by Page et al Virulence 2013
http://www.ncbi.nlm.nih.gov/pubmed/23669075
Which is very well written and offers a nice overview
Article Biomarkers of endothelial activation/dysfunction in infectio...
sE-selectin is a marker of early endothelial activation/damage in both the pulmonary and systemic circulations, so maybe a good bet in addition to ICAM-1 and vWF. We have obtained pretty good signals in human ARDS and inhaled LPS models, with vWF being the less sensitive of the three markers.
Thanks very much, Charlotte, Marco, Vilma, Nadine, Thomas, Jacek, Meddahi, etc. Very useful info. I'll check the references.
We did research in the past in Uni. Heidelberg. sICAM-1 is the best marker to indicate the prognosis of sepsis. Logically, it implies the importance of this marker to indicate endothelial activation.
I don't think soluble adhesion molecules (sICAM-1 and sVCAM-1) will be useful for you. In the type of critical patient you describe, with likely infections and established inflammation, these markers are probably constitutively present. I think it will be better for you to study a marker of more profound endothelial injury, such as soluble thrombomodulin (sTM). In fact, there is an excellent paper in the current Jan 15 issue of Semin Thromb Hemost by Maria Johansen et al, describing the power of sTM to predict impending organ failure and death in sepsis.
With regard to sTM, one always has to remember that injured hepatocytes are a very important and abundant source of the circulating molecule (see some of reaserch papers from myself). It limits the use of sTM as an endothelial activation/injury marker, especially in sepsis and multiorgan failure where liver is commonly affected.
Dear I support the idea of ICAM-1 as the most sensitive marker.
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