The DOI matches its Crossref record; 203 of the 203 references it cites were found in a registry or an index.
Recognition of Staphylococcus aureus by the Innate Immune System
Open accessAbstract
SUMMARY: The gram-positive bacterium Staphylococcus aureus is a major pathogen responsible for a variety of diseases ranging from minor skin infections to life-threatening conditions such as sepsis. Cell wall-associated and secreted proteins (e.g., protein A, hemolysins, and phenol-soluble modulin) and cell wall components (e.g., peptidoglycan and alanylated lipoteichoic acid) have been shown to be inflammatory, and these staphylococcal components may contribute to sepsis. On the host side, many host factors have been implicated in the innate detection of staphylococcal components. One class of pattern recognition molecules, Toll-like receptor 2, has been shown to function as the transmembrane component involved in the detection of staphylococcal lipoteichoic acid and phenol-soluble modulin and is involved in the synthesis of inflammatory cytokines by monocytes/macrophages in response to these components. Nod2 (nucleotide-binding oligomerization domain 2) is the intracellular sensor for muramyl dipeptide, the minimal bioactive structure of peptidoglycan, and it may contribute to the innate immune defense against S. aureus. The staphylococcal virulence factor protein A was recently shown to interact directly with tumor necrosis factor receptor 1 in airway epithelium and to reproduce the effects of tumor necrosis factor alpha. Finally, peptidoglycan recognition protein L is an amidase that inactivates the proinflammatory activities of peptidoglycan. However, peptidoglycan recognition protein L probably plays a minor role in the innate immune response to S. aureus. Thus, several innate immunity receptors may be implicated in host defense against S. aureus.
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Cites
The chemokine system in diverse forms of macrophage activation and polarization
MANTOVANI, A., SICA, A., SOZZANI, S., ALLAVENA, P., VECCHI, A., & LOCATI, M. (2004) · Trends in Immunology · doi:10.1016/j.it.2004.09.015 · Cited by 6,534
A Toll-like receptor recognizes bacterial DNA
Hemmi, H., Takeuchi, O., Kawai, T., Kaisho, T., Sato, S., Sanjo, H., Matsumoto, M., Hoshino, K., Wagner, H., Takeda, K., et al. (2000) · Nature · doi:10.1038/35047123 · Cited by 6,491
Staphylococcus aureus Infections
Lowy, F. D. (1998) · New England Journal of Medicine · doi:10.1056/nejm199808203390806 · Cited by 6,005
Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease
Hugot, J.-P., Chamaillard, M., Zouali, H., Lesage, S., Cézard, J.-P., Belaiche, J., Almer, S., Tysk, C., O'Morain, C. A., Gassull, M., et al. (2001) · Nature · doi:10.1038/35079107 · Cited by 5,591
A human homologue of the Drosophila Toll protein signals activation of adaptive immunity
Medzhitov, R., Preston-Hurlburt, P., & Janeway, C. A. (1997) · Nature · doi:10.1038/41131 · Cited by 5,590
A frameshift mutation in NOD2 associated with susceptibility to Crohn's disease
Ogura, Y., Bonen, D. K., Inohara, N., Nicolae, D. L., Chen, F. F., Ramos, R., Britton, H., Moran, T., Karaliuskas, R., Duerr, R. H., et al. (2001) · Nature · doi:10.1038/35079114 · Cited by 5,030
Toll-like receptors: critical proteins linking innate and acquired immunity
Akira, S., Takeda, K., & Kaisho, T. (2001) · Nature Immunology · doi:10.1038/90609 · Cited by 4,777
Peptidoglycan types of bacterial cell walls and their taxonomic implications
Schleifer, K. H., & Kandler, O. (1972) · Bacteriological Reviews · doi:10.1128/br.36.4.407-477.1972 · Cited by 4,222
Lemaitre, B., Nicolas, E., Michaut, L., Reichhart, J.-M., & Hoffmann, J. A. (1996) · Cell · doi:10.1016/s0092-8674(00)80172-5 · Cited by 4,043
CD14, a Receptor for Complexes of Lipopolysaccharide (LPS) and LPS Binding Protein
Wright, S. D., Ramos, R. A., Tobias, P. S., Ulevitch, R. J., & Mathison, J. C. (1990) · Science · doi:10.1126/science.1698311 · Cited by 3,987
Cited by
Staphylococcus aureus Biofilms Prevent Macrophage Phagocytosis and Attenuate Inflammation In Vivo
Thurlow, L. R., Hanke, M. L., Fritz, T., Angle, A., Aldrich, A., Williams, S. H., Engebretsen, I. L., Bayles, K. W., Horswill, A. R., & Kielian, T. (2011) · The Journal of Immunology · doi:10.4049/jimmunol.1002794 · Cited by 704
Clauditz, A., Resch, A., Wieland, K.-P., Peschel, A., & Götz, F. (2006) · Infection and Immunity · doi:10.1128/iai.00204-06 · Cited by 509
Immunity against Staphylococcus aureus cutaneous infections
Miller, L. S., & Cho, J. S. (2011) · Nature Reviews Immunology · doi:10.1038/nri3010 · Cited by 434
NOD2/CARD15 Mediates Induction of the Antimicrobial Peptide Human Beta-defensin-2
Voss, E., Wehkamp, J., Wehkamp, K., Stange, E. F., Schröder, J. M., & Harder, J. (2006) · Journal of Biological Chemistry · doi:10.1074/jbc.m511044200 · Cited by 344
The Role of Macrophages in Staphylococcus aureus Infection
Pidwill, G. R., Gibson, J. F., Cole, J., Renshaw, S. A., & Foster, S. J. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2020.620339 · Cited by 341
Metadata
- Authors
- Fournier, B., & Philpott, D. J.
- Venue
- Clinical Microbiology Reviews
- Publisher
- American Society for Microbiology
- Published
- 2005-07
- Volume
- 18
- Issue
- 3
- Pages
- 521-540
- ISSN
- 0893-8512 (ISSN-L)
- 1098-6618
- OpenAlex
- W2124145819
- Cited by
- 477
- References
- 203
- FWCI
- 5.47
- Type
- journal article
- Language
- en
- Open access
- green
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