Gut microbiota seems to be implicated in the atherosclerotic process. Translocation of bacterial endotoxins, like lipopolysaccharide (LPS) from gut to systemic circulation is being considered a new player contributing to chronic inflammation and atherosclerosis complications. Furthermore, endotoxins may have a role in platelet activation upon interaction with Toll-like receptor 4 (TLR4).
Until now, little is known about its role in the coronary thrombosis.
To explore this issue, we will compare LPS concentration and biomarkers of platelet activation in coronary thrombus and intra-coronary blood of patients with myocardial infarction and stable coronary disease respectively. Furthermore, to substantiate that LPS may be biologically active in the context, we will perform immune-histochemical analyses to investigate if TLR 4 is actually expressed at thrombus site
Serum levels of bacterial LPS, sP-selectin, a marker of platelet activation, and zonulin, a marker of gut permeability, will be measured in patients with ST-elevation myocardial infarction (STEMI) (n=50), stable coronary disease (n=50) and control subjects, matched for age, sex and cardiovascular risk factors (n=50). Serum LPS, soluble TLR4, a marker of TLR4 activation and sP-selectin will be also measured in coronary thrombi and coronary blood of patients with STEMI and stable coronary disease, respectively.
Finally, immuno-histochemical analysis will be performed to detect LPS and TLR4 activity in coronary thrombi.
If our hypothesis will be confirmed, LPS from gut microbiota could be be considered a novel and important trigger for platelet activation at the site of plaque rupture and a potential target for new therapies to counteract athero-thrombosis.
