Group A Streptococcal Adherence
- PMID: 26866229
- Bookshelf ID: NBK333427
Group A Streptococcal Adherence
Excerpt
Streptococcus pyogenes (group A streptococci) is an exclusive human pathogen that causes a wide range of infections, from acute pharyngitis and impetigo to life-threatening necrotizing fasciitis. The attachment of S. pyogenes to the pharyngeal and skin epithelial cell surfaces represents a critical first step in establishing such infections. While the importance of particular surface-exposed adhesins tends to be serotype- or infection-model–specific, adherence to human cells is generally regarded as a two-step process. The first step involves a relatively weak interaction mediated by lipoteichoic acid that allows the bacteria to overcome electrostatic repulsion. This initial interaction is followed by a stronger, more specific, and irreversible binding of a variety of tissue-specific protein or carbohydrate receptors to streptococcal surface molecules. This chapter reviews a number of the well-characterized streptococcal adherence mechanisms and will summarize some of the major advances that have been made in our understanding of this initial stage of infection.
© The University of Oklahoma Health Sciences Center.
Sections
- Abstract
- Lipoteichoic Acid
- M protein
- Pili
- Fibronectin binding proteins
- Protein F1 (SfbI)
- Protein F2, PFBP and FbaB
-
Serum Opacity Factor (SOF, SfbII) and
S. pyogenes fibronectin-binding protein X (SfbX) - M protein as a fibronectin binding protein and protein H
- Fbp54
- Streptococcal hemoprotein receptor (Shr)
- SDH/GAPDH binds to fibronectin and other eukaryotic receptors
- Streptococcal collagen-like proteins
- Hyaluronic acid capsule
- Laminin binding proteins
- FbaA
- Streptococcal surface enolase (SEN)
- Transcriptional changes during adherence
- References
References
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- Abbot E. L., Smith W. D., Siou G. P., Chiriboga C., Smith R. J., Wilson J. A., et al. Pili mediate specific adhesion of Streptococcus pyogenes to human tonsil and skin. Cell Microbiology. 2007;9(7):1822–1833. - PubMed
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