Abstract
Better understanding the mechanisms of Leonurus cardiaca L. extract (LCE) activity is necessary to prepare recommendations for the use of LCE-based herbal products for preventive/supportive purposes in case of infective endocarditis (IE) and other staphylococcal invasive infections. The aim of the study was to analyze molecular mechanisms of LCE effect on Staphylococcus aureus and blood platelets in the context of their interactions playing a pivotal role in such disorders. Using atomic force microscopy, we demonstrated that adhesion forces of S. aureus were markedly reduced after exposure to LCE at subinhibitory concentrations. The effect resulted from the impact of LCE on S. aureus cell morphology and the composition of phospholipids and fatty acids in bacterial membranes (assessed by HPLC), which modulated their stabilization, hydrophobicity, and charge. Moreover, using FACS we showed also that LCE significantly reduced GP IIb/IIIa expression on blood platelets, thus the disruption of platelet-fibrinogen interactions seems to explain antiplatelet effect of LCE. The obtained results prove the usefulness of LCE in the prevention of S. aureus adhesion, platelet activation, and vegetations development, however, also pointed out the necessity of excluding the cationic antibiotics from the treatment of S. aureus-associated IE and other invasive diseases, when motherwort herb is used simultaneously as an addition to the daily diet.
Highlights
Infective endocarditis (IE) is an acute, life-threatening disease, in which microbial colonization leads to progressive damage of heart tissue via the formation of complex aggregates called vegetations containing microbes, fibrin, activated platelets, and phagocytes
In our studiesconcentrations we demonstrated unknown antiadhesive endocarditis in vitroeffects model
It can be assumed that the observed changes in the composition of phospholipids and fatty acids in the presence of L. extract extract (LCE), followed by membrane charge, fluidity, and hydrophobicity, at least partially determine the adhesive properties of S. aureus cells, leading to the desired effects such as reduction of adhesion forces measured using single-bacterial contact probe atomic force microscopy, and inhibition both of staphylococcal adhesion and biofilm formation, which we demonstrated previously [12,14]
Summary
Infective endocarditis (IE) is an acute, life-threatening disease, in which microbial colonization leads to progressive damage of heart tissue (usually valves) via the formation of complex aggregates called vegetations containing microbes, fibrin, activated platelets, and phagocytes. A (SpA), and secretory proteins such as coagulase (Coa) or von Willebrand factor binding protein (vWbp) participate in S. aureus adherence, biofilm formation, and myocardial/endovascular diseases development [2,4,5]. Due to their complex structure and physiology, biofilms enhance microbial cell survival under environmental stress conditions, including exposure to antimicrobials and the components of host immune system.
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