Staphylococcus epidermidis–fibronectin binding and its inhibition by heparin

Arciola, Carla Renata; Bustanji, Yasser; Conti, Matteo; Campoccia, Davide; Baldassarri, Lucilla; Samorı̀, Bruno; Montanaro, Lucio

doi:10.1016/s0142-9612(03)00133-9

Cited by 85 publications

(56 citation statements)

References 27 publications

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“…Similar results were reported by Arciola et al [33] and Nilsdotter-Augustinsson et al [34]. Nevertheless the inability of the tested S. epidermidis isolates to adhere to collagen disagrees with results reported by Wadstrom et al [35].…”

Section: Discussionsupporting

confidence: 82%

Role of different classes of mammalian cell surface molecules in adherence of coagulase positive and coagulase negative staphylococci

Hafez

Aboulwafa

Yassien

et al. 2008

J. Basic Microbiol.

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In the present study the role of different mammalian cell receptors in adherence of the coagulase positive pathogen, Staphylococcus aureus and some coagulase negative staphylococci, namely Staphylococcus epidermidis and Staphylococcus saprophyticus was investigated. Upon testing the adherence to Vero and Hep-2 cells, S. aureus isolates showed an adherence to both cell lines while S. epidermidis and S. saprophyticus isolates adhered to Vero cells only. According to the obtained results, both O-linked and N-linked mammalian cell surface glycoproteins are involved in the adherence of S. aureus isolates to Vero and Hep-2 cells, whereas only the O-linked ones serve as receptors for adherence of S. epidermidis and S. saprophyticus isolates to Vero cells. Of the O-linked glycoproteins, GAG-like receptors are involved in adherence of all tested isolates to Vero cells. The coagulase positive staphylococci preferred to adhere to the highly sulphated GAGs (Heparin and chondroitin sulphate B) while the coagulase negative isolates showed higher affinity to the less sulphated ones (Chondroitin sulphate A and C). Mucin like receptors appeared to be important for the adherence of all tested staphylococci. The role exhibited by fibronectin- and fibrinogen-like receptors was detected with S. aureus and S. epidermidis but not with S. saprophyticus isolates. While, collagen and gelatin were found to contribute to the adherence of S. aureus isolates only. Neither carbohydrate moieties of the glycoconjugates nor lipid molecules on the mammalian cell surface played a role in the adherence of the tested staphylococcal isolates. Taken together, the results revealed that both coagulase negative and coagulase positive staphylococcal tested isolates adhere to the same classes of mammalian cell surface receptors such as mucin-like, fibrinogen-like, fibronectin-like and GAG-like receptors. However, the tested isolates exhibited different degrees of affinities to such receptors.

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Section: Discussionsupporting

confidence: 82%

Role of different classes of mammalian cell surface molecules in adherence of coagulase positive and coagulase negative staphylococci

Hafez

Aboulwafa

Yassien

et al. 2008

J. Basic Microbiol.

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“…aureus fibronectin binding proteins have heparin binding domains, and it has been reported that the addition of exogenous heparin results in the inability of these proteins to participate in adherence to fibronectin-coated coverslips (3,67). We predicted that if fibronectin binding proteins are required for citrate-stimulated biofilm formation, then the addition of heparin could disrupt the ability of the cells to aggregate.…”

Section: Resultsmentioning

confidence: 96%

Genetic Evidence for an Alternative Citrate-Dependent Biofilm Formation Pathway in Staphylococcus aureus That Is Dependent on Fibronectin Binding Proteins and the GraRS Two-Component Regulatory System

et al. 2008

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We reported previously that low concentrations of sodium citrate strongly promote biofilm formation by Staphylococcus aureus laboratory strains and clinical isolates. Here, we show that citrate promotes biofilm formation via stimulating both cell-to-surface and cell-to-cell interactions. Citrate-stimulated biofilm formation is independent of the ica locus, and in fact, citrate represses polysaccharide adhesin production. We show that fibronectin binding proteins FnbA and FnbB and the global regulator SarA, which positively regulates fnbA and fnbB gene expression, are required for citrate's positive effects on biofilm formation, and citrate also stimulates fnbA and fnbB gene expression. Biofilm formation is also stimulated by several other tricarboxylic acid (TCA) cycle intermediates in an FnbA-dependent fashion. While aconitase contributes to biofilm formation in the absence of TCA cycle intermediates, it is not required for biofilm stimulation by these compounds. Furthermore, the GraRS two-component regulator and the GraRS-regulated efflux pump VraFG, identified for their roles in intermediate vancomycin resistance, are required for citrate-stimulated cell-to-cell interactions, but the GraRS regulatory system does not impact the expression of the fnbA and fnbB genes. Our data suggest that distinct genetic factors are required for the early steps in citrate-stimulated biofilm formation. Given the role of FnbA/FnbB and SarA in virulence in vivo and the lack of a role for ica-mediated biofilm formation in S. aureus catheter models of infection, we propose that the citrate-stimulated biofilm formation pathway may represent a clinically relevant pathway for the formation of these bacterial communities on medical implants.Microorganisms commonly adhere to surfaces in multilayered groupings referred to as biofilms (29,54). Growth in a biofilm imparts particular properties to member organisms, including elevated levels of resistance to antibiotics and host defenses. Staphylococcus aureus, a common nosocomial pathogen known for its antibiotic resistance and its ability to cause a wide range of infections (43), can form biofilms on a number of medically relevant surfaces such as catheters and intraocular lenses (56,71,75). Biofilm formation by this microbe is thought to contribute to its ability to cause persistent infections (19,71,74).Most genetic studies of biofilm formation by S. aureus have involved the search for biofilm-defective mutants using laboratory medium, typically tryptic soy broth (TSB) supplemented with glucose. Such an approach has identified a number of genetic loci required for biofilm formation, including sarA, agr, dlt, hla, clp, and ica, which codes for the polysaccharide component of an extracellular biofilm matrix (9,25,27,45,55,66,72). The ica locus, its gene products, and the polysaccharide produced by the Ica proteins have been studied extensively in vitro (17, 44-46, 50, 53). A recent study reported a role for the ica locus of S. aureus in models of systemic infection and renal abscess infect...

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“…Among those is protein A on S. aureus which binds to the tumor necrosis factor α receptor on osteoblasts [46, 47]. Others include fibronectin-binding proteins which are expressed by bacteria and mediate binding to surface-associated fibronectin on osteoblasts [48–50]. Because S. aureus uses a different binding site on fibronectin as S. epidermidis , different signalling pathways are triggered, which could explain that synthesis of CXCL2 is stimulated by S. aureus , but that of CCL3 is not.…”

Section: Discussionmentioning

confidence: 99%

The Macrophage Inflammatory Proteins MIP1α(CCL3) and MIP2α(CXCL2) in Implant-Associated Osteomyelitis: Linking Inflammation to Bone Degradation

Dapunt

Maurer

Giese

et al. 2014

Mediators of Inflammation

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Bacterial infections of bones remain a serious complication of endoprosthetic surgery. These infections are difficult to treat, because many bacterial species form biofilms on implants, which are relatively resistant towards antibiotics. Bacterial biofilms elicit a progressive local inflammatory response, resulting in tissue damage and bone degradation. In the majority of patients, replacement of the prosthesis is required. To address the question of how the local inflammatory response is linked to bone degradation, tissue samples were taken during surgery and gene expression of the macrophage inflammatory proteins MIP1α (CCL3) and MIP2α (CXCL2) was assessed by quantitative RT-PCR. MIPs were expressed predominantly at osteolytic sites, in close correlation with CD14 which was used as marker for monocytes/macrophages. Colocalisation of MIPs with monocytic cells could be confirmed by histology. In vitro experiments revealed that, aside from monocytic cells, also osteoblasts were capable of MIP production when stimulated with bacteria; moreover, CCL3 induced the differentiation of monocytes to osteoclasts. In conclusion, the multifunctional chemokines CCL3 and CXCL2 are produced locally in response to bacterial infection of bones. In addition to their well described chemokine activity, these cytokines can induce generation of bone resorbing osteoclasts, thus providing a link between bacterial infection and osteolysis.

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Staphylococcus epidermidis–fibronectin binding and its inhibition by heparin

Cited by 85 publications

References 27 publications

Role of different classes of mammalian cell surface molecules in adherence of coagulase positive and coagulase negative staphylococci

Role of different classes of mammalian cell surface molecules in adherence of coagulase positive and coagulase negative staphylococci

Genetic Evidence for an Alternative Citrate-Dependent Biofilm Formation Pathway in Staphylococcus aureus That Is Dependent on Fibronectin Binding Proteins and the GraRS Two-Component Regulatory System

The Macrophage Inflammatory Proteins MIP1α(CCL3) and MIP2α(CXCL2) in Implant-Associated Osteomyelitis: Linking Inflammation to Bone Degradation

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