Prophylaxis of Experimental Endocarditis With Antiplatelet and Antithrombin Agents: A Role for Long-term Prevention of Infective Endocarditis in Humans?

Veloso, Tiago Rafael; Que, Yok-Ai; Chaouch, Aziz; Giddey, Marlyse; Vouillamoz, Jacques; Rousson, Valentin; Moreillon, Philippe; Entenza, José M.

doi:10.1093/infdis/jiu426

Cited by 49 publications

(49 citation statements)

References 47 publications

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“…Platelets play a pivotal role in the progression and development of IE, but their role can be likened to a double-edged sword (185)(186)(187)(188). Platelets display both haemostatic and host defence properties.…”

Section: Innate Host Responsementioning

confidence: 99%

Biofilms and host response – helpful or harmful

Moser

Pedersen

Lerche

et al. 2017

APMIS

124

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host response -helpful or harmful. APMIS 2017; 125: 320-338.Biofilm infections are one of the modern medical world's greatest challenges. Probably, all non-obligate intracellular bacteria and fungi can establish biofilms. In addition, there are numerous biofilm-related infections, both foreign bodyrelated and non-foreign body-related. Although biofilm infections can present in numerous ways, one common feature is involvement of the host response with significant impact on the course. A special characteristic is the synergy of the innate and the acquired immune responses for the induced pathology. Here, we review the impact of the host response for the course of biofilm infections, with special focus on cystic fibrosis, chronic wounds and infective endocarditis.

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Section: Innate Host Responsementioning

confidence: 99%

Biofilms and host response – helpful or harmful

Moser

Pedersen

Lerche

et al. 2017

APMIS

124

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“…Platelet-rich plasma (PRP) and platelet-poor plasma (PPP) for platelet aggregation tests were obtained from anticoagulated human blood as described previously (29).…”

Section: Methodsmentioning

confidence: 99%

“…The ability of sera from immunized rats to inhibit S. gordonii-induced platelet aggregation was evaluated in vitro by conventional light aggregometry as previously described (29). Briefly, 20 l of S. gordonii (final concentration of 1 ϫ 10 9 CFU/ml in Tyrode's buffer) was preincubated for 1 h at room temperature with 2 l of control or anti-Hsa-, anti-PadA-, and anti-Hsa-plus anti-PadA-containing sera and then added to 180 l of PRP in siliconized flat-bottom cuvettes.…”

Section: Methodsmentioning

confidence: 99%

Antibodies Targeting Hsa and PadA Prevent Platelet Aggregation and Protect Rats against Experimental Endocarditis Induced by Streptococcus gordonii

et al. 2016

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Streptococcus gordonii and related species of oral viridans group streptococci (VGS) are common etiological agents of infective endocarditis (IE). We explored vaccination as a strategy to prevent VGS-IE, using a novel antigen-presenting system based on non-genetically modified Lactococcus lactis displaying vaccinogens on its surface. Hsa and PadA are surface-located S. gordonii proteins implicated in platelet adhesion and aggregation, which are key steps in the pathogenesis of IE. This function makes them ideal targets for vaccination against VGS-IE. In the present study, we report the use of nonliving L. lactis displaying at its surface the N-terminal region of Hsa or PadA by means of the cell wall binding domain of Lactobacillus casei A2 phage lysine LysA2 (Hsa-LysA2 and PadA-LysA2, respectively) and investigation of their ability to elicit antibodies in rats and to protect them from S. gordonii experimental IE. Immunized and control animals with catheter-induced sterile aortic valve vegetations were inoculated with 10 6 CFU of S. gordonii. The presence of IE was evaluated 24 h later. Immunization of rats with L. lactis HsaLysA2, L. lactis PadA-LysA2, or both protected 6/11 (55%), 6/11 (55%), and 11/12 (91%) animals, respectively, from S. gordonii IE (P < 0.05 versus controls). Protection correlated with the induction of high levels of functional antibodies against both Hsa and PadA that delayed or totally inhibited platelet aggregation by S. gordonii. These results support the value of L. lactis as a system for antigen delivery and of Hsa and PadA as promising candidates for a vaccine against VGS-IE.

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“…99 It was recently shown that treatment with the thrombin and staphylothrombin inhibitor dabigatran could protect against the development of S. aureus endocarditis in rats. 100 Establishment of IE requires adhesion to the vessel wall under high shear stress conditions. The interaction of S. aureus vWbp with VWF, either attached to the subendothelium or released by inflamed endothelial cells, is sufficient to mediate adhesion in flow conditions in vivo.…”

Section: Staphylothrombin and Infective Endocarditismentioning

confidence: 99%

Coagulase Activity by Staphylococcus aureus: A Potential Target for Therapy?

Peetermans

Verhamme

Vanassche

2015

Semin Thromb Hemost

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Staphylococcus aureus is a leading cause of skin and soft tissue infections, foreign body infections, and infective endocarditis. In case of endovascular infection with S. aureus, higher rates of cardiac valve destruction, embolic complications, severe sepsis, and death occur. The unique capacity of S. aureus to induce clotting has been known for over a century; however, its role in virulence has long been controversial. S. aureus secretes two coagulases, staphylocoagulase and von Willebrand factor binding protein that both activate prothrombin to generate fibrin. A better understanding of the molecular mechanisms as well as the new strategies to target the coagulases have highlighted their importance in S. aureus virulence. Coagulase activity is essential for the formation of S. aureus-fibrin-platelet microaggregates and for the homing of S. aureus to the vascular wall under flow. Absence or inhibition of S. aureus coagulase activity improved outcome in disease models of skin infection, sepsis, catheter infection, and endocarditis. Here, we review how the manipulation of the host's hemostatic system contributes to the disease-causing potential of S. aureus and discuss the S. aureus coagulases as promising targets for novel therapeutic strategies.

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Prophylaxis of Experimental Endocarditis With Antiplatelet and Antithrombin Agents: A Role for Long-term Prevention of Infective Endocarditis in Humans?

Cited by 49 publications

References 47 publications

Biofilms and host response – helpful or harmful

Biofilms and host response – helpful or harmful

Antibodies Targeting Hsa and PadA Prevent Platelet Aggregation and Protect Rats against Experimental Endocarditis Induced by Streptococcus gordonii

Coagulase Activity by Staphylococcus aureus: A Potential Target for Therapy?

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