Mouse models of endotoxemia (such as an LPS injection) are associated with increased cell death. Such as increases in cell death seen in the spleen.
In human patients with endotoxemia I think cell death is also observed. However, I am unsure where it occurs, to what degree, what cells? What similarities are there to the mouse model?
I would assume there is. However, I don't know any critical-care clinical pathologists to whom I can pose this puzzler.
I can mention that this 12 year old article by L. Moldawer makes reference to cell death in humans; http://www.fasebj.org/content/15/6/879.long Back then it was of course referred to as apoptosis. Which, IMO is a just a general term used by many people for cell death.
What new information is out there regarding cell death observed in humans? Are there any existing treatments which attempt to address/prevent cell death in human clinical endotoxemia (assuming it is looked for)?
I cannot provide you direct answer but we did have a paper in Pediatr Res 2002 about human neutrophil and endotoxin induced apoptosis. Apoptosis was more in neutrophil from premature babies. I was told that extracorporeal membrane oxygenator (ECMO) with a filter in place can help taking out the endotoxin. Hope my limited information can help you.
Endotoxinemai ist difficult to measure - therefore no direct relationship but indirectly, procalcitonien levels (pct) indicate general lps stimulation in the body and pct levels show som ecorrelation with outcome
Agree with Hans-Dieter Volk. In contrast to murine endotoxaemia, in human no standardization may be achieved. We had several studies of LPS, EndoCAb, cytokines, and apoptosis markers as well, etc. in both humans and rats. Comparing is difficult as humans have disease status when raised LPS is only a part of condition, while in rodents we use industry made LPS with standardized source, activity, etc. PCT, lactate, total cholesterol or other markers are useless when trying to achieve direct effect of LPS. Furthermore, LPS-binding protein influences the pro-apoptotic effect of LPS multiple times. Same levels of serum LPS under different conditions (for example, sepsis, IBD or fatty liver disease in our studies) cause different levels of apoptosis.