Alterations in lipoprotein homeostasis during human experimental endotoxemia and clinical sepsis.
Level 3 - non-randomized controlled study
Non-randomized human experimental challenge study with an intervention arm and observational clinical cohort
PubMed 17980169 · doi:10.1016/j.bbalip.2007.10.001
What was done
The study evaluated sequential changes in lipoprotein composition and lipid transfer/binding proteins (LCAT, CETP, PLTP) in clinical sepsis and in human subjects undergoing low-dose experimental endotoxemia (LPS). It also assessed the effect of infusing reconstituted HDL (rHDL) prior to low-dose LPS administration compared to LPS infusion alone.
What was found
The abstract reports no numerical values or statistical metrics, stating only qualitative findings: in clinical sepsis, CRP correlated negatively with LCAT and CETP activities, and positively with PLTP activity and LPS binding protein. Following LPS infusion alone, PLTP activity decreased and LCAT activity slightly decreased. Infusion of rHDL prior to LPS caused a transient increase in PLTP activity, a slight decrease in LCAT activity, long-lasting increases in HDL cholesterol and apo A-I, and high initial processing of phosphatidylcholine and lyso-PC, though overall plasma lipid changes were comparable to the LPS-only control.
Why it matters
It demonstrates that acute systemic inflammation shifts lipid transfer protein dynamics depending on the stimulus magnitude, and that pre-treatment with rHDL extensively remodels circulating lipoproteins without preventing general acute-phase lipid alterations.
Limits
The abstract provides no sample size (n is unreported), participant demographics, or baseline clinical details. No quantitative effect sizes, variance measures, or p-values are given. Experimental endotoxemia is a brief, controlled model that does not replicate the duration and severity of clinical sepsis.
Cited by
- supports Cholesterol components can act as acute-phase reactants that change acutely in response to stress and inflammation.