Wall Teichoic Acid in Staphylococcus aureus Host Interaction
Staphylococcus aureus is a major opportunistic human pathogen that frequently causes disease in community and hospital settings. Nasal colonization is an important risk factor for developing invasive disease. Cell wall-associated glycopolymers called wall teichoic acids (WTAs) contribute to efficien...
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Veröffentlicht in: | Trends in microbiology (Regular ed.) 2020-12, Vol.28 (12), p.985-998 |
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Sprache: | eng |
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Zusammenfassung: | Staphylococcus aureus is a major opportunistic human pathogen that frequently causes disease in community and hospital settings. Nasal colonization is an important risk factor for developing invasive disease. Cell wall-associated glycopolymers called wall teichoic acids (WTAs) contribute to efficient nasal colonization by S. aureus. In addition, WTAs are key targets of the host immune system due to their accessibility and high abundance on the S. aureus cell surface. In this review we discuss the new insights into interactions between the host and S. aureus WTA and the implications of these interactions for preventative and therapeutic approaches against S. aureus-mediated disease.
Staphylococcus aureus is a major human pathogen. The cell wall glycopolymer wall teichoic acid (WTA) contributes to nasal colonization and immune interaction by S. aureus.Human immune receptors from multiple classes recognize glycan modifications on S. aureus WTA. These include surface-expressed receptors on immune cells [langerin and macrophage galactose-type lectin (MGL)], scavenger receptors (SREC-1), and soluble receptors in serum [specific antibodies and mannose-binding lectin (MBL)].Dissection of the functional consequences of WTA–receptor interactions should provide insight into protective versus evasive responses. Unfortunately, as some of these interactions show species specificity, the use of mouse models to assess their contribution to infection is limited.S. aureus WTA is an interesting target for therapeutic and preventative approaches, such as antibody therapy, phage therapy, and vaccination. |
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ISSN: | 0966-842X 1878-4380 |
DOI: | 10.1016/j.tim.2020.05.017 |