A family of putative MSCRAMMs from Enterococcus faecalis

Abstract

The recently published Enterococcus faecalis genome [Paulsen, I. T., Banerjei, L., Myers, G. S. & 29 other authors (2003). Science 299, 2071–2074)] was examined and 41 putative cell-wall-anchored proteins were identified. Seventeen of these proteins are predicted to contain tandemly repeated immunoglobulin-like folds characteristic of the structural organization of staphylococcal adhesins of the MSCRAMM (microbial surface component recognizing adhesive matrix molecules) type. Two of the nine proteins selected for further study appear to represent cell-wall-anchored enzymes. It is proposed that the remaining seven proteins constitute a family of structurally related proteins potentially interacting with proteins of the host. This family includes the previously identified collagen/laminin-binding MSCRAMM ACE [Rich, R. L., Kreikemeyer, B., Owens, R. T., LaBrenz, S., Narayana, S. V., Weinstock, G. M., Murray, B. E. & Hook, M. (1999). J Biol Chem 274, 26939–26945]. It is further demonstrated that genes encoding the seven putative MSCRAMMs are present in all E. faecalis strains tested and these proteins appear to be expressed during infection in humans, since sera from infected individuals contain antibodies reacting with recombinant versions of the enterococcal proteins.

Fibronectin Binding and Proteolytic Degradation byLeishmaniaand Effects on Macrophage Activation

“…Various microbial pathogens also express cell surface proteins (microbial surface components recognizing adhesive matrix molecules) which promote binding to ECM and BM proteins (23,27,28). Thus, our findings support the idea that cutaneous Leishmania species express a receptor protein functionally analogous to microbial surface components recognizing adhesive matrix molecules.…”

Vancomycin-Resistant Enterococcus faecalis Endocarditis: Linezolid Failure and Strain Characterization of Virulence Factors

“…Ace is a specific collagen-binding adhesin of the MSCRAMM family, has been identified in E. faecalis endocarditis isolates (17), and mediates attachment of E. faecalis to collagen types I and IV and laminin (18). Subsequently, a family of seven genes encoding MSCRAMM-like proteins was found in 100% (nine out of nine) of the E. faecalis endocarditis strains tested, and elevated titers of IgG to these MSCRAMMlike proteins were found in the sera of nine patients with E. faecalis infections (27). Three of these genes, ebpA, ebpB, and ebpC (endocarditis-and biofilm-associated pili), control sur- face pilus formation and may be important in endocarditis pathogenesis (16).…”

“…E. faecalis strains recovered from patients with endocarditis have a greater capacity to adhere to Girardi heart cells than to urinary tract epithelial cells in vitro (6), which suggests that adherence to vascular endothelium may be important. MSCRAMMs mediate binding of bacteria to extracellular matrix proteins and function as adhesins to damaged heart tissue (17,18,27). Ace is a specific collagen-binding adhesin of the MSCRAMM family, has been identified in E. faecalis endocarditis isolates (17), and mediates attachment of E. faecalis to collagen types I and IV and laminin (18).…”

“…These included the gelatinase gene (22,26,28,30); recently described pilus-encoding genes (16); genes encoding putative MSCRAMMs (microbial surface components recognizing adhesive matrix molecules) with predicted immunoglobulin (Ig)-like folds (17,18,27; J. Sillanpää, S. R. Nallapareddy, and B. E. Murray, unpublished data); genes, including esp (33), in a predicted pathogenicity island (PAI) (15); and an acquired gene that contributes to biofilm formation (32) ( Table 1). The strain was examined for phenotypic production of gelatinase (22), hemolytic activity on Bacto Tryptic Soy Agar (Becton Dickinson and Company, Sparks, MD) plus 5% human blood agar plates, and biofilm formation (14).…”

Insights into the biofilm lifestyle of enterococci

“…17 Interestingly, genes encoding a predicted transcriptional regulator (EF1090) and a sortase C protein (EF1094) flanked these genes. Loss of any of these genes resulted in a variety of phenotypes including, loss of biofilm development, loss of pili formation and attenuation in endocarditis and ascending urinary tract infection animal models.…”