Adhesion of staphylococcus aureus to fibrinogen, collagen and lectin in relation to cell surface structure

Ohtomo, Toshichika; Yoshida, Kenichi

doi:10.1016/s0176-6724(88)80017-8

Cited by 8 publications

(10 citation statements)

References 37 publications

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“…Indeed, Kiser et al (19) demonstrated that a mutant defective in CP5 production colonized the nares of mice as well as the parental strain at 1 week, but it showed reduced levels of colonization 2 weeks after inoculation. Furthermore, CP1 and CP2 have been implicated in the masking of cell surface adhesins (11,14,33). Thus, CP5 and CP8 may not have a role in initial colonization, but they may play a role during spreading from the initial site to the secondary sites.…”

Section: Discussionmentioning

confidence: 99%

Regulation of Staphylococcus aureus Capsular Polysaccharide Expression by agr and sarA

Luong

Gómez

et al. 2002

Infect Immun

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This study addresses the regulation of Staphylococcus aureus type 8 capsular polysaccharide (CP8) expression by the global regulators agr and sarA. We analyzed CP8 production, cap8-specific mRNA synthesis, and blaZ reporter gene activities of the transcriptional and translational fusions in strain Becker and its agr, sarA, and agr-sarA isogenic mutants during different phases of bacterial growth. In the wild-type strain, cap8 mRNA was undetectable until the mid-logarithmic phase of growth, whereas CP8 production was undetectable until 2 h later, at the onset of stationary phase. The delay most likely reflects the time needed for completing CP8 synthesis resulting from translation of cap8 mRNA. The agr mutation caused drastic reductions in CP8 production and cap8 gene transcription, suggesting that agr is a major positive regulator of CP8 expression. The results of gene fusion studies indicated that regulation by agr is exerted at the transcriptional level. In contrast, the sarA mutation caused only a slight reduction in cap8 mRNA synthesis and reporter gene activities. By comparing CP8 production and cap8 transcription, we observed that sarA affected CP8 production both trancriptionally and posttranslationally. We showed that agr was a major activator for cap gene expression not only in type 8 strain Becker but also in strains representing the four agr groups.More than 90% of Staphylococcus aureus strains produce capsular polysaccharide (CP). Eleven serotypes of staphylococcal CP have been identified, but only CP type 1 (CP1), CP2, CP5, and CP8 have been chemically characterized. CP1 and CP2 have been shown to be antiphagocytic virulence factors. Strains producing CP1 and CP2 are heavily encapsulated; however, these strains are rarely isolated clinically. In fact, more than 80% of clinical isolates produce either CP5 or CP8 (see reference 23 for a review). Recently, CP5 has been shown to play an important role in the pathogenesis of S. aureus, most probably by allowing the organism to resist uptake and killing by phagocytes (1,27,43). Because of their prevalence, CP5 and CP8 have been used as targets for vaccine development, and specific antibodies against CP5 and CP8 have been shown to be protective against S. aureus infections (13, 24).The cap1, cap5, and cap8 gene clusters, required for the synthesis of CP1, CP5, and CP8, respectively, have been cloned and sequenced. The cap5 and cap8 operons are allelic, whereas the cap1 locus is located at a different location. Twelve of the 16 genes in the cap5 and cap8 operons have high degrees of similarity, which reflects the fact that the repeating units of CP5 and CP8 are almost identical (23). Transcriptional analyses have shown that all 16 genes of the cap8 locus are transcribed as a large transcript from a major promoter upstream of the first gene, cap8A. Although several internal promoters within the cap8 gene cluster have also been identified by genetic complementation and reporter gene fusion studies, these internal promoters are much weaker than the primary pro...

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Section: Discussionmentioning

confidence: 99%

Regulation of Staphylococcus aureus Capsular Polysaccharide Expression by agr and sarA

Luong

Gómez

et al. 2002

Infect Immun

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“…Previous studies have shown that the expression of S. aureus extracellular polysaccharide(s) interferes with the adherence process by masking adhesins (8,18,20,(42)(43)(44)50). However, masking was seen only for heavily encapsulated strains belonging to capsular type 1 or 2 or was due to an uncharacterized capsule-like material detected after growth of strains in milk whey (43).…”

Section: Discussionmentioning

confidence: 99%

Adherence ofStaphylococcus aureusto Endothelial Cells: Influence of Capsular Polysaccharide, Global Regulatoragr, and Bacterial Growth Phase

et al. 2000

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The adherence of Staphylococcus aureus to human endothelial cells (EC) is probably an important step in the pathogenesis of systemic staphylococcal infections. We examined the influence of type 5 capsular polysaccharide (CP5) production, the global regulator agr, and the bacterial growth phase on S. aureus adherence to EC. Whereas S. aureus Newman showed maximal adherence to EC in the logarithmic phase of growth, an isogenic agr mutant showed maximal adherence in the stationary growth phase. S. aureus adherence to EC and CP5 expression were negatively correlated: a mutation in the agr locus diminished CP5 production and led to increased adherence. Likewise, induction of CP5 expression by addition of NaCl to the growth medium resulted in reduced staphylococcal adherence to EC. S. aureus Newman cells that adhered to EC did not express CP5. A Newman cap5O mutant was acapsular and showed significantly greater adherence to EC than the parental strain did (P < 0.005). Complementation of the cap5O mutation in trans restored CP5 expression and reduced EC adherence to a level similar to that of the parental strain. The enhanced adherence shown by the cap5O mutant was similar in magnitude to that of the agr mutant or the cap5O agr double mutant. Cells of the cap5O mutant and cap5O agr double mutant harvested from stationary-phase cultures adhered significantly better than did cells harvested in the exponential growth phase. These data are consistent with the postexponential and agr-independent expression by S. aureus of at least one putative EC adhesin, whose binding domain may be masked by CP5.Staphylococcus aureus is responsible for a broad range of human diseases, including foreign body infections, bacteremia, abscesses, and wound infections (41). The ability of S. aureus to adhere to extracellular matrix proteins is thought to be essential for colonization and the establishment of infections (17, 41, 52). The interaction of S. aureus with endothelial cells (EC) may play a major role in the pathogenesis of endovascular infections, including endocarditis and metastatic infections (26,41).S. aureus can express several cell wall-associated adhesins specific for recognizing matrix proteins; these adhesins are referred to as MSCRAMMs (microbial surface components recognizing adhesive matrix molecules) (52). MSCRAMMs with specific binding activity toward fibronectin (31, 62), fibrinogen (45, 47), and collagen (53) have been cloned and biochemically characterized. Whether MSCRAMMs are also responsible for the adherence of S. aureus to host cells is still unclear. A role for fibronectin-binding proteins in staphylococcal adherence to bovine epithelial cells (13) and mammary gland cells (36) was recently described; however, other factors were also postulated to mediate epithelial cell adherence (13).The expression of most cell wall adhesins and extracellular virulence determinants in S. aureus is coordinately regulated during the growth cycle (57). Some of the growth cycle-dependent expression patterns can be attributed to the ...

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“…Staphylococcus aureus is a pathogen frequently involved in device-centered infections and has been shown to bind specifically to a variety of plasma proteins, 18,19,30,34 including fibrinogen 3,18,19,23,31,34 and fibronectin. 19,24,36,43 Clumping factor has been shown to be the primary receptor involved in the binding of the Newman strain of Staphylococcus aureus to surfaces coated with purified fibrinogen 7,28,29 or with plasma 7 in vitro, suggesting a possible molecular mechanism for bacterial adhesion, and subsequent infection, to biomaterial surfaces in vivo.…”

Section: Introductionmentioning

confidence: 99%

Quantitative comparison of shear-dependentStaphylococcus aureus adhesion to three polyurethane ionomer analogs with distinct surface properties

Dickinson

Nagel

Proctor

et al. 1997

J. Biomed. Mater. Res.

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Bacterial adhesion is a central step in infection on biomaterial surfaces; however, the relation between biomaterial surface properties and adhesion remains poorly understood. To quantitatively determine the relationship among polyurethane surface properties, protein coating, and adhesion, we have compared attachment and detachment kinetics of Staphylococcus aureus on three different novel polyurethanes with different protein coatings. Rate constants for attachment or detachment were measured as a function of shear rate in a well-defined laminar flow field. The tested polyurethanes included a relatively hydrophobic-base polyether urethane and hydrophilic anionomer and cationomer analogs of the base material. Materials were tested bare, or coated with human fibrinogen, plasma, or albumin. The results suggest that the presence of fibrinogen or plasma greatly enhance the attachment rate constants and decrease the detachment rate constants on all materials. The most extreme differences among the different materials were observed on the bare materials, with the base polyurethane being most resistant to both attachment and detachment. However, except for a reduced attachment rate constant on the plasma-coated sulfonated polyurethane, few differences in the rate constants were observed among protein-coated materials, suggesting the primary role of surface properties is masked by the presence of the adsorbed protein layer.

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Adhesion of staphylococcus aureus to fibrinogen, collagen and lectin in relation to cell surface structure

Cited by 8 publications

References 37 publications

Regulation of Staphylococcus aureus Capsular Polysaccharide Expression by agr and sarA

Regulation of Staphylococcus aureus Capsular Polysaccharide Expression by agr and sarA

Adherence ofStaphylococcus aureusto Endothelial Cells: Influence of Capsular Polysaccharide, Global Regulatoragr, and Bacterial Growth Phase

Quantitative comparison of shear-dependentStaphylococcus aureus adhesion to three polyurethane ionomer analogs with distinct surface properties

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