Pro-inflammatory cytokines IL6, TNF-α, IL1β, procalcitonin, lipopolysaccharide binding protein and C-reactive protein in infective endocarditis

Watkin, Richard; Harper, Lucy V; Vernallis, Ann B.; Lang, Susan; Lambert, Peter A.; Ranasinghe, AM; Elliott, Tom

doi:10.1016/j.jinf.2007.05.174

Cited by 51 publications

(41 citation statements)

References 26 publications

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“…FnbpA was shown to trigger the uptake of L. lactis (and S. aureus) by endothelial cells (16,18,38). Collectively, these results compared well with the elevated levels of IL-1␤ and IL-6 observed after internalization of S. aureus by endothelial cells in vitro (20) and in patients with S. aureus IE (39)(40)(41). Previous studies by Dankert el al.…”

Section: Discussionsupporting

confidence: 70%

Use of a Human-Like Low-Grade Bacteremia Model of Experimental Endocarditis To Study the Role of Staphylococcus aureus Adhesins and Platelet Aggregation in Early Endocarditis

et al. 2013

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Section: Discussionsupporting

confidence: 70%

Use of a Human-Like Low-Grade Bacteremia Model of Experimental Endocarditis To Study the Role of Staphylococcus aureus Adhesins and Platelet Aggregation in Early Endocarditis

et al. 2013

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“…33 On systemic inflammation, ADAMTS13 is consumed by overwhelming amounts of VWF released into the blood, 13 suggesting also a reduced concentration of ADAMTS13 in the course of endocarditis. In addition, it has been proposed that interleukin 6, which was found to be elevated in the blood of endocarditis patients, 34 could block ADAMTS13 activity. To understand the role of ADAMTS13 for the ULVWF-mediated adhesion of S aureus, we analyzed bacterial attachment in the presence of platelets and inactivated serum supplemented with different amounts of recombinant ADAMTS13 (n=4) or serum with a physiological ADAMTS13 activity (n=4).…”

Section: Bacterial Binding Is Affected By Platelets and Adamts13mentioning

confidence: 99%

Ultralarge von Willebrand Factor Fibers Mediate Luminal Staphylococcus aureus Adhesion to an Intact Endothelial Cell Layer Under Shear Stress

et al. 2013

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50S taphylococcus aureus is a major pathogen responsible for various infections in humans and is the most frequent cause of infective endocarditis in industrialized countries. 1 Prerequisite for the pathogenesis of infective endocarditis is infection of the endocardium.2 Therefore, one of the first and essential steps is bacterial adhesion to the endothelium. In contrast to other pathogens causing infective endocarditis, S. aureus appears to be able to bind not only to damaged but also to intact endothelium. [3][4][5] Fibrinogen, fibronectin, and platelets, in combination with S aureus clumping factor and fibronectin-binding proteins, are involved in the pathogenesis of infective endocarditis. [6][7][8] In addition, wall teichoic acids of S aureus have been implicated in adhesion to the endothelial cell (EC) layer. 9 However, the molecular mechanisms of the very first adhesion steps of S aureus to the undamaged endothelium are still largely unknown.Background-During pathogenesis of infective endocarditis, Staphylococcus aureus adherence often occurs without identifiable preexisting heart disease. However, molecular mechanisms mediating initial bacterial adhesion to morphologically intact endocardium are largely unknown. Methods and Results-Perfusion of activated human endothelial cells with fluorescent bacteria under high-shear-rate conditions revealed 95% attachment of the S aureus by ultralarge von Willebrand factor (ULVWF). Flow experiments with VWF deletion mutants and heparin indicate a contribution of the A-type domains of VWF to bacterial binding. In this context, analyses of different bacterial deletion mutants suggest the involvement of wall teichoic acid but not of staphylococcal protein A. The presence of inactivated platelets and serum increased significantly ULVWF-mediated bacterial adherence. ADAMTS13 (a disintegrin and metalloproteinase with thrombospondin motifs 13) caused a dose-dependent reduction of bacterial binding and a reduced length of ULVWF, but single cocci were still tethered by ULVWF at physiological levels of ADAMTS13. To further prove the role of VWF in vivo, we compared wild-type mice with VWF knockout mice. Binding of fluorescent bacteria was followed in tumor necrosis factor-α-stimulated tissue by intravital microscopy applying the dorsal skinfold chamber model. Compared with wild-type mice (n=6), we found less bacteria in postcapillary (60±6 versus 32±5 bacteria) and collecting venules (48±5 versus 18±4 bacteria; P<0.05) of VWF knockout mice (n=5). Conclusions-Our data provide the first evidence that ULVWF contributes to the initial pathogenic step of S aureusinduced endocarditis in patients with an apparently intact endothelium. An intervention reducing the ULVWF formation with heparin or ADAMTS13 suggests novel therapeutic options to prevent infective endocarditis. Clinical Perspective on p 59Recruitment of host cells to the endothelium is a crucial step during inflammation and coagulation. It has been shown previously that under shear von Willebrand factor is a potent bindi...

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“…In this context, the availability of biomarkers is of major interest. Several studies have investigated the application and usefulness of important laboratory markers for IE diagnosis (5)(6)(7)(8)(9)(10)(11)(12). Other studies (13)(14)(15)(16) have focused on the clinical usefulness of serum Creactive protein (CRP), a marker most frequently used in Europe (13 ), in IE.…”

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confidence: 99%

Lipopolysaccharide-Binding Protein: A New Biomarker for Infectious Endocarditis?

et al. 2009

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Background: Infectious endocarditis (IE) is a bacterial infection of the endocardium. Diagnosis is based on results obtained from echocardiography, blood cultures, and molecular genetic screening for bacteria and on data for inflammatory markers such as the leukocyte (WBC) count and the C-reactive protein (CRP) concentration. The aim of the present study was to evaluate lipopolysaccharide-binding protein (LBP) as a supportive biomarker for the diagnosis and therapeutic monitoring of IE. Methods: We measured LBP and CRP concentrations and WBC counts in 57 IE patients at hospital admission, 40 patients with noninfectious heart valve diseases (HVDs), and 55 healthy blood donors. The progression of these 3 markers and the influence of cardiac surgery on them were evaluated in 29 IE patients and 21 control patients. Results: Serum LBP concentrations were significantly higher in IE patients [mean (SD), 33.41 (32.10) mg/L] compared with HVD patients [6.67 (1.82) mg/L, P < 0.0001] and healthy control individuals [5.61 (1.20) mg/L]. The progression in the LBP concentration during therapy of IE patients correlated with the changes in the CRP concentration. The 2 markers were equally influenced by antibiotic treatment and surgical intervention. Conclusions: Serial LBP measurement may provide an effective and useful tool for evaluating the response to therapy in IE patients. We found a strong correlation between LBP and CRP concentrations; LBP has a tendency to increase earlier in cases of reinfection.

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Pro-inflammatory cytokines IL6, TNF-α, IL1β, procalcitonin, lipopolysaccharide binding protein and C-reactive protein in infective endocarditis

Cited by 51 publications

References 26 publications

Use of a Human-Like Low-Grade Bacteremia Model of Experimental Endocarditis To Study the Role of Staphylococcus aureus Adhesins and Platelet Aggregation in Early Endocarditis

Use of a Human-Like Low-Grade Bacteremia Model of Experimental Endocarditis To Study the Role of Staphylococcus aureus Adhesins and Platelet Aggregation in Early Endocarditis

Ultralarge von Willebrand Factor Fibers Mediate Luminal Staphylococcus aureus Adhesion to an Intact Endothelial Cell Layer Under Shear Stress

Lipopolysaccharide-Binding Protein: A New Biomarker for Infectious Endocarditis?

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