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Infective endocarditis (IE) after the implantation of a bovine jugular vein (BJV) graft in the right ventricular outflow tract has recently been described to be more frequent than for other conduits.
were the first to study bacterial adhesion to different tissues in vitro; their clinical bacterial isolates displayed increased adherence to BJV valves, as compared with bovine and porcine pericardium, especially in traumatized valve leaflets. As discussed in their accompanying letter, we have presented results somewhat incongruous with their findings by claiming that the surface composition of the conduits, bacterial surface proteins, and shear forces per se are not the most important determinants of bacterial adherence in vitro.
In this study, we primarily investigated whether (1) morphologic tissue differences, (2) bacterial species specificity, (3) exposure to extracellular substrates, and (4) stasis versus shear stress determine bacterial adhesiveness to the graft tissues investigated. However, as an advantage, in vitro models allow investigations in a comprehensive way, building up (patho)physiological complexity, progressively including more in vivo determinants.
that clinical bacterial isolates may be more virulent than our reference strains and that the experimental setup influenced testing of bacterial adhesion in static or flow conditions. Nevertheless, the same Staphylococcus aureus, Staphylococcus epidermidis, and Streptococcus sanguis “lab” strains were tested in previous in vitro studies and manifested the full pathogenic spectrum of S aureus, ie, activation of endothelial proinflammatory and procoagulant pathways, crucial in the onset of IE.
Fibrin- and collagen-based matrices attenuate inflammatory and procoagulant responses in human endothelial cell cultures exposed to Staphylococcus aureus.
In addition to the adhesive factors presently studied, it is also determined by plasma proteins, platelets, and inflammatory cells to allow formation of a vegetation, indeed consisting mainly of fibrin and bacteria. In agreement with Jalal and colleagues,
we admit that the exact in vivo conditions are difficult to replicate in an experimental setup and that IE models are required that will enable a more complex environment needed to better understand the mechanisms behind the clinical observations.
Therefore, to progressively evaluate factors present in the “in vivo status,” as a first step, we have investigated the role of plasma proteins in bacterial adhesion to tissues in our flow models. First results show that fibrinogen adsorption was greater for the BJV tissue compared with the cryopreserved homograft tissue (Figure 1). We speculate that surface-bound fibrinogen might facilitate subsequent bacterial adhesion, as fibrin(ogen), together with fibronectin are known key players for the adhesion of IE-associated pathogens to traumatized endothelium or medical devices.
we appreciate that further efforts will have to be undertaken to investigate the impact of plasma proteins, blood cells, and rheological factors on bacterial adhesiveness in conditions of laminar and turbulent flow. Such an approach may in turn foster the option of adequate IE-preventive therapy and limit IE-associated risks to help increase patients' quality of life.
References
Malekzadeh-Milani S.
Ladouceur M.
Patel M.
Boughenou F.M.
Iserin L.
Bonnet D.
et al.
Incidence and predictors of Melody(R) valve endocarditis: a prospective study.
Fibrin- and collagen-based matrices attenuate inflammatory and procoagulant responses in human endothelial cell cultures exposed to Staphylococcus aureus.
We read with great interest the work published by Veloso and colleagues1 that investigated the bacterial adherence to pulmonary valve graft tissues under static and flow conditions. These experiments were achieved using wild bacterial strains of Staphylococcus aureus, Staphylococcus epidermidis, and Streptococcus sanguinis and the following valvular substrates: bovine pericardium patch, bovine jugular vein, and cryopreserved homograft. The authors concluded that the surface composition of bovine jugular vein and homograft tissues themselves, bacterial surface proteins, and shear forces per se were not the prime determinants of bacterial adherence.
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