The Role of Platelets in Infective Endocarditis

Braï, Mustapha Abdeljalil; Hannachi, Nadji; Gueddari, Nabila El; Baudoin, Jean-Pierre; Dahmani, Abderrhamane; Lépidi, Hubert; Habib, Gilbert; Camoin-Jau, Laurence

doi:10.3390/ijms24087540

Cited by 5 publications

(4 citation statements)

References 122 publications

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“…For example, the P2Y12 platelet receptor antagonist ticagrelor could couple its potent and well-known antiplatelet role with noticeable antibacterial properties. Furthermore, a recent study based on a mouse animal model reported a pronounced capacity of ticagrelor to eradicate S. aureus bacteremia [ 131 , 132 , 133 , 134 , 135 ] ( Table 3 ).…”

Section: Resultsmentioning

confidence: 99%

Host–Bacterium Interaction Mechanisms in Staphylococcus aureus Endocarditis: A Systematic Review

Nappi

Singh

2023

IJMS

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Staphylococci sp. are the most commonly associated pathogens in infective endocarditis, especially within high-income nations. This along with the increasing burden of healthcare, aging populations, and the protracted infection courses, contribute to a significant challenge for healthcare systems. A systematic review was conducted using relevant search criteria from PubMed, Ovid’s version of MEDLINE, and EMBASE, and data were tabulated from randomized controlled trials (RCT), observational cohort studies, meta-analysis, and basic research articles. The review was registered with the OSF register of systematic reviews and followed the PRISMA reporting guidelines. Thirty-five studies met the inclusion criteria and were included in the final systematic review. The role of Staphylococcus aureus and its interaction with the protective shield and host protection functions was identified and highlighted in several studies. The interaction between infective endocarditis pathogens, vascular endothelium, and blood constituents was also explored, giving rise to the potential use of antiplatelets as preventative and/or curative agents. Several factors allow Staphylococcus aureus infections to proliferate within the host with numerous promoting and perpetuating agents. The complex interaction with the hosts’ innate immunity also potentiates its virulence. The goal of this study is to attain a better understanding on the molecular pathways involved in infective endocarditis supported by S. aureus and whether therapeutic avenues for the prevention and treatment of IE can be obtained. The use of antibiotic-treated allogeneic tissues have marked antibacterial action, thereby becoming the ideal substitute in native and prosthetic valvular infections. However, the development of effective vaccines against S. aureus still requires in-depth studies.

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Section: Resultsmentioning

confidence: 99%

Host–Bacterium Interaction Mechanisms in Staphylococcus aureus Endocarditis: A Systematic Review

Nappi

Singh

2023

IJMS

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“…It provides insights into the relationships between the A1 domain of VWF multimers, platelets, neutrophils, and NETs under conditions of high and low shear flow (indicated by red and blue arrows, respectively). Abbreviations: AS, aggregation substance; Clf, clumping factor; Ebp, endocarditis- and biofilm-associated pili; FcγR, crystallisable fragment gamma receptor; Fg, ds, double strand; fibrinogen; Fn, fibronectin; FnBP, fibronectin-binding protein; GP, glycoprotei; GspB, Streptococcus gordonii surface platelet B; IgG, immunoglobulin G; IsdB, iron-responsive surface determinant B; PadA, platelet adherence protein A; Sar P, staphylococcal accessory regulator protein; SrpA, serine-rich glycoprotein A; SRR-1, serine-rich repeat glycoprotein 1; SSL5, staphylococcal superantigen-like 5; VWF, von Willebrand factor [ 128 , 129 , 130 , 131 , 132 , 133 , 134 , 135 , 136 , 137 , 138 , 139 , 140 , 141 , 142 , 143 , 144 ].…”

Section: Figurementioning

confidence: 99%

“…This concept offers an intriguing explanation. Several studies have confirmed that the endocardium is indeed a modified endothelium [143][144][145][146][147], although there has been some uncertainty about the specifics of endocardial development. E. faecalis can directly colonise different host epithelial surfaces in a variety of animal experimental models.…”

Section: The Role Of the Endocardium And Enterococcal Pathoadaptationmentioning

confidence: 99%

Current Knowledge of Enterococcal Endocarditis: A Disease Lurking in Plain Sight of Health Providers

Nappi

2024

Pathogens

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Enterococcus faecalis is a bacterial pathogen that can cause opportunistic infections. Studies indicate that initial biofilm formation plays a crucial regulatory role in these infections, as well as in colonising and maintaining the gastrointestinal tract as a commensal member of the microbiome of most land animals. It has long been thought that vegetation of endocarditis resulting from bacterial attachment to the endocardial endothelium requires some pre-existing tissue damage, and in animal models of experimental endocarditis, mechanical valve damage is typically induced by cardiac catheterisation preceding infection. This section reviews historical and contemporary animal model studies that demonstrate the ability of E. faecalis to colonise the undamaged endovascular endothelial surface directly and produce robust microcolony biofilms encapsulated within a bacterially derived extracellular matrix. This report reviews both previous and current animal model studies demonstrating the resilient capacity of E. faecalis to colonise the undamaged endovascular endothelial surface directly and produce robust microcolony biofilms encapsulated in a bacterially derived extracellular matrix. The article also considers the morphological similarities when these biofilms develop on different host sites, such as when E. faecalis colonises the gastrointestinal epithelium as a commensal member of the common vertebrate microbiome, lurking in plain sight and transmitting systemic infection. These phenotypes may enable the organism to survive as an unrecognised infection in asymptomatic subjects, providing an infectious resource for subsequent clinical process of endocarditis.

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“…The known pathophysiology of IE is one example of how the immune system has a connection with the hemostatic system. The endothelial lining of the heart and its valves are normally resistant to infection with bacteria and fungi and maintain their functions [ 10 , 11 ]. Conversely, the formation of valve vegetation may be induced by a damaged or inflamed endothelium [ 12 , 13 , 14 ].…”

Section: Introductionmentioning

confidence: 99%

Understanding Bartonella-Associated Infective Endocarditis: Examining Heart Valve and Vegetation Appearance and the Role of Neutrophilic Leukocytes

Meidrops,

Groma,

Goldins

et al. 2023

Cells

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Background. The endocardium and cardiac valves undergo severe impact during infective endocarditis (IE), and the formation of vegetation places IE patients at a heightened risk of embolic complications and mortality. The relevant literature indicates that 50% of IE cases exhibit structurally normal cardiac valves, with no preceding history of heart valve disease. Gram-positive cocci emerge as the predominant causative microorganisms in IE, while Gram-negative Bartonella spp., persisting in the endothelium, follow pathogenic pathways distinct from those of typical IE-causing agents. Employing clinical as well as advanced microbiological and molecular assays facilitated the identification of causative pathogens, and various morphological methods were applied to evaluate heart valve damage, shedding light on the role of neutrophilic leukocytes in host defense. In this research, the immunohistochemical analysis of neutrophilic leukocyte activation markers such as myeloperoxidase, neutrophil elastase, calprotectin, and histone H3, was performed. A distinct difference in the expression patterns of these markers was observed when comparing Bartonella spp.-caused and non-Bartonella spp.-caused IE. The markers exhibited significantly higher expression in non-Bartonella spp.-caused IE compared to Bartonella spp.-caused IE, and they were more prevalent in vegetation than in the valvular leaflets. Notably, the expression of these markers in all IE cases significantly differed from that in control samples. Furthermore, we advocated the use of 16S rRNA Next-Generation Sequencing on excised heart valves as an effective diagnostic tool for IE, particularly in cases where blood cultures yielded negative results. The compelling results achieved in this study regarding the enigmatic nature of Bartonella spp. IE’s pathophysiology contribute significantly to our understanding of the peculiarities of inflammation and immune responses.

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The Role of Platelets in Infective Endocarditis

Cited by 5 publications

References 122 publications

Host–Bacterium Interaction Mechanisms in Staphylococcus aureus Endocarditis: A Systematic Review

Host–Bacterium Interaction Mechanisms in Staphylococcus aureus Endocarditis: A Systematic Review

Current Knowledge of Enterococcal Endocarditis: A Disease Lurking in Plain Sight of Health Providers

Understanding Bartonella-Associated Infective Endocarditis: Examining Heart Valve and Vegetation Appearance and the Role of Neutrophilic Leukocytes

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