Infection of human endothelial cells with<i>Staphylococcus aureus</i>induces the production of monocyte chemotactic protein-1 (MCP-1) and monocyte chemotaxis

Tekstra, Janneke; Beekhuizen, Henry; Gevel, Joke S. van de; Benten, I.J. van; Tuk, Cornelis W.; Beelen, Robert H.J.

doi:10.1046/j.1365-2249.1999.01002.x

Cited by 41 publications

(53 citation statements)

References 35 publications

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“…We previously reported that S. aureus upon internalization by EC induces monocyte adhesion and chemotaxis by increasing EC surface expression of ICAM-1 and VCAM-1 molecules (9) and secretion of MCP-1 (40). In extension to this, the present study shows a similar response of EC after infection with S. epidermidis or S. sanguis.…”

Section: Discussionsupporting

confidence: 85%

“…Our previous studies demonstrated that virulent as well as less virulent S. aureus organisms and to a lesser extent S. sanguis and S. epidermidis infect and colonize EC in culture (9,40,43). As a result of infection with S. aureus, but not S. sanguis or S. epidermidis, EC are activated to express TF mRNA, TF surface antigen, and TFA (43).…”

Section: Discussionmentioning

confidence: 99%

“…The bacteria used in this study were S. aureus 42D, S. epidermidis ATCC 149900, and S. sanguis NCTC 7864 and have been used extensively in our previous studies of BE (2,3,40,43). Bacteria suspensions were stored at Ϫ70°C and prepared for use as described previously (43).…”

Section: Reagentsmentioning

confidence: 99%

“…Adding to the results of studies by other investigators (5,25,32), we found that S. aureus, a pathogen with a high propensity to colonize endocardial tissue and to cause infections of intact heart valves, binds to and is actively internalized by cultured human EC (9,43,45). As a result, virulent S. aureus strains caused direct EC damage but less virulent strains induced EC activation that resulted in the production of a variety of proinflammatory mediators, including interleukin-1 (IL-1), IL-6, IL-8, monocyte chemotactic protein 1 (MCP-1), and RANTES (9,40,48,49), surface membrane expression of intercellular adhesion molecule 1 (ICAM-1; CD54) and vascular cell adhesion molecule 1 (VCAM-1; CD106), and monocyte adhesion. S. aureus-infected EC also expressed TFA, which was controlled at the level of TF gene transcription and TF protein synthesis and was synergistically enhanced by IL-1, a representative cytokine released during bacteremia (43).…”

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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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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: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Section: Reagentsmentioning

confidence: 99%

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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“…Of those genes that were differentially regulated, ICAM-1 and MCP-1 are interesting candidates for further study, as these molecules may act as part of an inflammatory host response to infection (71)(72)(73). ICAM-1 is an inducible cell adhesion glycoprotein of the Ig supergene family expressed on the surface of a wide variety of cell types (74), and may be up-regulated in response to proinflammatory cytokines, hormones, cellular stresses, and virus infection to promote intercellular signaling during inflammation (75).…”

Section: Discussionmentioning

confidence: 99%

Corneal IL-8 Expression Following Adenovirus Infection Is Mediated by c-Src Activation in Human Corneal Fibroblasts

Natarajan

Rajala

Chodosh

2003

The Journal of Immunology

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Emerging evidence indicates that intracellular signaling cascades mediate entry of pathogenic adenoviruses into target host cells as well as some of the undesirable inflammatory responses to adenoviral gene vectors. We found that Ad19 infection of cultured human corneal fibroblasts induced IL-8 gene transcription independently of IL-1β, TNF-α, and viral gene expression, suggesting that intracellular signaling events might mediate early inflammatory events in adenovirus keratitis. Heat but not UV light inactivation of the virus abrogated the effect of infection on IL-8 mRNA and protein levels, consistent with a viral binding-mediated mechanism. The tyrosine kinase inhibitor herbimycin blocked Ad19-induced IL-8 expression. Western blot analysis revealed tyrosine phosphorylation of the functionally related kinases c-Src and extracellular signal-regulated kinase (ERK) 1/2 in corneal fibroblasts within 15 min after infection. Respective inhibitors of these kinases, PP2 and PD98059, also blocked Ad19-induced IL-8 mRNA and protein expression. Application of inhibitors to Src and ERK kinase assays suggested an upstream relationship of c-Src to ERK. Finally, DNA microarray studies performed 1 h after Ad19 or mock infection of corneal fibroblasts in the presence or absence of the Src-specific inhibitor PP2 confirmed a relationship between c-Src and IL-8 expression in Ad19-infected corneal cells. c-Src may act as a global regulator of early proinflammatory host responses to Ad19 infection of the human cornea.

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Pathogen interactions with endothelial cells and the induction of innate and adaptive immunity

Konradt

Hunter

2018

Eur J Immunol

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There are over 10 trillion endothelial cells (EC) that line the vasculature of the human body. These cells not only have specialized functions in the maintenance of homeostasis within the circulation and various tissues but they also have a major role in immune function. EC also represent an important replicative niche for a subset of viral, bacterial, and parasitic organisms that are present in the blood or lymph; however, there are major gaps in our knowledge regarding how pathogens interact with EC and how this influences disease outcome. In this article, we review the literature on EC-pathogen interactions and their role in innate and adaptive mechanisms of resistance to infection and highlight opportunities to address prominent knowledge gaps.

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Infection of human endothelial cells withStaphylococcus aureusinduces the production of monocyte chemotactic protein-1 (MCP-1) and monocyte chemotaxis

Cited by 41 publications

References 35 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

Corneal IL-8 Expression Following Adenovirus Infection Is Mediated by c-Src Activation in Human Corneal Fibroblasts

Pathogen interactions with endothelial cells and the induction of innate and adaptive immunity

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