Role of Monocytes in Experimental
            <i>Staphylococcus aureus</i>
            Endocarditis

Veltrop, Marcel H. A. M.; Bancsi, Maurice J. L. M. F.; Bertina, Rogier M.; Thompson, J.

doi:10.1128/iai.68.8.4818-4821.2000

Cited by 36 publications

(38 citation statements)

References 19 publications

(17 reference statements)

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“…Ultimately, monocytes, which settle from the circulatory system onto these infected endocardial lesions, are activated to express TFA (1-3, 44). This result will intensify the deposit of fibrin clots on the endocardial surface (2,3,44), ultimately causing heart dysfunction.…”

Section: Discussionmentioning

confidence: 99%

“…Subsequent in vivo experiments with the rabbit model of BE revealed that TF needed to maintain fibrin formation was generated by monocytes from the circulatory system settling on the fibrin of growing (infected) vegetations (2,3,44). Also, in vitro, human monocytes generated increased levels of TF-dependent procoagulant activity (TFA) upon binding to fibrin containing bacteria, in particular S. aureus, S. sanguis, or S. epidermidis (1)(2)(3)44).…”

mentioning

confidence: 99%

“…Many clinical and experimental studies on the pathogenesis of BE gave clear insight into the processes in vegetations that are already formed on mechanically damaged valvular endocardium. In this stage of the disease the procoagulant molecule tissue factor (TF) is required to activate the clotting system and maintain fibrin deposition (2,3,44). TF is a 47-kDa transmembrane glycoprotein that in complex with coagulation factor VIIa (FVIIa) acts as a serine protease and cleaves factor X (FX).…”

mentioning

confidence: 99%

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Monocytes Augment Bacterial Species- and Strain-Dependent Induction of Tissue Factor Activity in Bacterium-Infected Human Vascular Endothelial Cells

2001

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In bacterial endocarditis (BE), intravascular infection with Staphylococcus aureus, Streptococcus sanguis, orStaphylococcus epidermidis can lead to formation of a fibrin clot on the inner surface of the heart and cause heart dysfunction. The events that start the coagulation in the early stage of the disease are largely unknown. We have recently shown that human endothelial cells (EC) upon binding and internalization of S. aureus, but not S. sanguis or S. epidermidis, express tissue factor (TF)-dependent procoagulant activity (TFA). The present study shows that infection of EC with these three pathogens induces surface expression of intracellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) and monocyte adhesion. Subsequent coculture of these cells synergistically enhanced TFA, which was exclusively dependent on TF molecules that were expressed on EC during coculture. TFA induction required direct contact between monocytes and bacterium-infected EC, but the signals for this response were not generated by the binding of monocytes through their ␤ 2 -or ␣ 4 -integrins to ICAM-1 or VCAM-1, respectively, on infected EC. The mechanism by which monocytes induce TFA in bacterium-infected EC was partly mediated by the proinflammatory cytokine interleukin-1 produced by the cells during coculture. Endogenous tumor necrosis factor alpha was not involved. This modulating effect of monocytes on species-and strain-dependent TFA of bacterium-infected EC supports our hypothesis that in an early stage in the pathogenesis of BE, as well as other intravascular infections that lead to detrimental fibrin formation, the coagulation cascade can be activated on the surfaces of EC as a consequence of specific interactions between pathogenic bacteria, EC, and monocytes.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Monocytes Augment Bacterial Species- and Strain-Dependent Induction of Tissue Factor Activity in Bacterium-Infected Human Vascular Endothelial Cells

2001

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“…H uman leukocytes play critical roles in the early detection and efficient removal of virulent pathogens during bacteremia via various surface receptors/receptor complexes (1). Similar to TLRs (2), C-type lectins (CLs) are essential in recognizing pathogens and alerting the host to elicit immune responses against bacterial (3), fungal (4), and viral infections (5).…”

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confidence: 99%

Secreted M-Ficolin Anchors onto Monocyte Transmembrane G Protein-Coupled Receptor 43 and Cross Talks with Plasma C-Reactive Protein to Mediate Immune Signaling and Regulate Host Defense

Zhang

Yang

Ang³

et al. 2010

The Journal of Immunology

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Although transmembrane C-type lectins (CLs) are known to initiate immune signaling, the participation and mechanism of action of soluble CLs have remained enigmatic. In this study, we found that M-ficolin, a conserved soluble CL of monocyte origin, overcomes its lack of membrane-anchor domain by docking constitutively onto a monocyte transmembrane receptor, G protein-coupled receptor 43 (GPCR43), to form a pathogen sensor-cum-signal transducer. On encountering microbial invaders, the M-ficolin–GPCR43 complex activates the NF-κB cascade to upregulate IL-8 production. We showed that mild acidosis at the local site of infection induces conformational changes in the M-ficolin molecule, which provokes a strong interaction between the C-reactive protein (CRP) and the M-ficolin–GPCR43 complex. The collaboration among CRP–M-ficolin–GPCR43 under acidosis curtails IL-8 production thus preventing immune overactivation. Therefore, we propose that a soluble CL may become membrane-associated through interaction with a transmembrane protein, whereupon infection collaborates with other plasma protein to transduce the infection signal and regulate host defense. Our finding implies a possible mechanism whereby the host might expand its repertoire of immune recognition-cum-regulation tactics by promiscuous protein networking. Furthermore, our identification of the pH-sensitive interfaces of M-ficolin–CRP provides a powerful template for future design of potential immunomodulators.

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“…Maximum activation was found at a bacterium-to-monocyte ratio of 9. Using a rabbit model, these workers showed that S. aureus [25] and Streptococcus sanguis [26,27] can also induce tissue factor activity on endocardial vegetations. In line with the present case, these workers proposed that tissue factor expression by monocytes might be more likely caused by indirect, rather than by direct, bacteria-monocyte interactions.…”

Section: Discussionmentioning

confidence: 99%

Very severe thrombocytopenia and fragmentation hemolysis mimicking thrombotic thrombocytopenic purpura associated with a giant intracardiac vegetation infected with Staphylococcus epidermidis: Role of monocyte procoagulant activity induced by bacterial supernatant

Selleng¹,

Warkentin²,

Greinacher³

et al. 2006

American J Hematol

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The pathogenesis of very severe thrombocytopenia in bacterial endocarditis is uncertain. We report a 50‐year‐old male with platelet counts < 10 × 109/l and fragmentation hemolysis complicating Staphyloccoccus epidermidis pacemaker endocarditis with a giant vegetation. Antibiotics, corticosteroids, high‐dose intravenous gammaglobulin, and plasmapheresis (for initially‐suspected thrombotic thrombocytopenic purpura) failed to produce significant platelet count increase. However, therapeutic‐dose heparin anticoagulation was associated with a platelet count increase from <10 to ∼40 × 109/l, with parallel reduction in thrombin‐antithrombin complexes (from 8.9 to 3.5 μg/l), facilitating surgical intervention. The thrombocytopenia promptly resolved following surgical removal of the vegetation. Culture supernatant from S. epidermidis isolated from the patient's blood induced monocytes to express procoagulant activity (assessed by factor Xa generation) equivalent to lipopolysaccharide (1 μg/ml), with half‐maximal activation seen with culture supernatant diluted to 1:12,800. These data are consistent with previous animal models of endocarditis demonstrating staphylococci‐induced procoagulant changes in monocytes. This case demonstrates that heparin anticoagulation can be therapeutic in infective endocarditis‐associated severe thrombocytopenia in a non‐bleeding patient, and that such therapy may ameliorate the platelet count enough to permit surgical intervention. Am. J. Hematol 2007. © 2006 Wiley‐Liss, Inc.

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Role of Monocytes in Experimental Staphylococcus aureus Endocarditis

Cited by 36 publications

References 19 publications

Monocytes Augment Bacterial Species- and Strain-Dependent Induction of Tissue Factor Activity in Bacterium-Infected Human Vascular Endothelial Cells

Monocytes Augment Bacterial Species- and Strain-Dependent Induction of Tissue Factor Activity in Bacterium-Infected Human Vascular Endothelial Cells

Secreted M-Ficolin Anchors onto Monocyte Transmembrane G Protein-Coupled Receptor 43 and Cross Talks with Plasma C-Reactive Protein to Mediate Immune Signaling and Regulate Host Defense

Very severe thrombocytopenia and fragmentation hemolysis mimicking thrombotic thrombocytopenic purpura associated with a giant intracardiac vegetation infected with Staphylococcus epidermidis: Role of monocyte procoagulant activity induced by bacterial supernatant

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