The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
Staphylococcal alpha-phenol soluble modulins contribute to neutrophil lysis after phagocytosis: S. aureus α-PSMs lyse neutrophils from within
Open accessAbstract
Staphylococcus aureus community-acquired (CA) MRSA strains are highly virulent and can cause infections in otherwise healthy individuals. The most important mechanism of the host for clearing S. aureus is phagocytosis by neutrophils and subsequent killing of the pathogen. Especially CA-MRSA strains are very efficient in circumventing this neutrophil killing. Interestingly, only a relative small number of virulence factors have been associated with CA-MRSA, one of which are the phenol soluble modulins (PSMs). We have recently shown that the PSMs are functionally inhibited by serum lipoproteins, indicating that PSMs may exert their cytolytic function primarily in the intracellular environment. To further investigate the intracellular role of the PSMs we measured the effect of the α-type and β-type PSMs on neutrophil killing after phagocytosis. Using fluorescently labelled S. aureus, we measured bacterial survival after phagocytosis in a plate reader, which was employed next to flow cytometry and time-lapse microscopy. Phagocytosis of the CA-MRSA strain MW2 by human neutrophils resulted in rapid host cell death. Using mutant strains of MW2, we demonstrated that in the presence of serum, the intracellular expression of only the psmα operon is both necessary and sufficient for both increased neutrophil cell death and increased survival of S. aureus. Our results identify PSMα peptides as prominent contributors to killing of neutrophils after phagocytosis, a finding with major implications for our understanding of S. aureus pathogenesis and strategies for S. aureus vaccine development.
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Cites
Waves of resistance: Staphylococcus aureus in the antibiotic era
Chambers, H. F., & DeLeo, F. R. (2009) · Nature Reviews Microbiology · doi:10.1038/nrmicro2200 · Cited by 2,718
Self-citationDavid, M. Z., & Daum, R. S. (2010) · Clinical Microbiology Reviews · doi:10.1128/cmr.00081-09 · Cited by 1,972
Wang, R., Braughton, K. R., Kretschmer, D., Bach, T.-H. L., Queck, S. Y., Li, M., Kennedy, A. D., Dorward, D. W., Klebanoff, S. J., Peschel, A., et al. (2007) · Nature Medicine · doi:10.1038/nm1656 · Cited by 1,046
Self-citationLiu, G. Y., Essex, A., Buchanan, J. T., Datta, V., Hoffman, H. M., Bastian, J. F., Fierer, J., & Nizet, V. (2005) · The Journal of Experimental Medicine · doi:10.1084/jem.20050846 · Cited by 752
Insights into Mechanisms Used by Staphylococcus aureus to Avoid Destruction by Human Neutrophils
Voyich, J. M., Braughton, K. R., Sturdevant, D. E., Whitney, A. R., Saïd-Salim, B., Porcella, S. F., Long, R. D., Dorward, D. W., Gardner, D. J., Kreiswirth, B. N., et al. (2005) · The Journal of Immunology · doi:10.4049/jimmunol.175.6.3907 · Cited by 563
Self-citationCogen, A. L., Yamasaki, K., Sanchez, K. M., Dorschner, R. A., Lai, Y., MacLeod, D. T., Torpey, J. W., Otto, M., Nizet, V., Kim, J. E., et al. (2010) · Journal of Investigative Dermatology · doi:10.1038/jid.2009.243 · Cited by 432 · cited 1×
“Multiple cell types can be lysed, liposomes can be perforated (Cogen et al., 2010) and genetic deletion of the PSMs impacts virulence in mice and rodents (Wang et al., 2007; Li et al., 2010).”
BackgroundSelf-citationNeutrophils in innate host defense against Staphylococcus aureus infections
Rigby, K. M., & DeLeo, F. R. (2012) · Seminars in Immunopathology · doi:10.1007/s00281-011-0295-3 · Cited by 400
Self-citationEvolution of virulence in epidemic community-associated methicillin-resistant Staphylococcus aureus
Li, M., Diep, B. A., Villaruz, A. E., Braughton, K. R., Jiang, X., DeLeo, F. R., Chambers, H. F., Lu, Y., & Otto, M. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0900743106 · Cited by 394 · cited 1×
“Although the PSM-encoding loci are conserved in the core genome of all sequenced staphylococcal strains, the in vitro expression correlates with the more virulent phenotype between CA-MRSA and HA-MRSA (Wang et al., 2007; Li et al., 2009).”
BackgroundSelf-citationCCR5 is a receptor for Staphylococcus aureus leukotoxin ED
Alonzo III, F., Kozhaya, L., Rawlings, S. A., Reyes-Robles, T., DuMont, A. L., Myszka, D. G., Landau, N. R., Unutmaz, D., & Torres, V. J. (2013) · Nature · doi:10.1038/nature11724 · Cited by 291
Wardenburg, J. B., Palazzolo‐Ballance, A. M., Otto, M., Schneewind, O., & DeLeo, F. R. (2008) · The Journal of Infectious Diseases · doi:10.1086/592053 · Cited by 236
Self-citation
Cited by
Yipp, B. G., & Kubes, P. (2013) · Blood · doi:10.1182/blood-2013-04-457671 · Cited by 989
Staphylococcus aureus Secreted Toxins and Extracellular Enzymes
Tam, K., & Torres, V. J. (2019) · Microbiology Spectrum · doi:10.1128/microbiolspec.gpp3-0039-2018 · Cited by 452
The Bicomponent Pore-Forming Leucocidins of Staphylococcus aureus
Alonzo, F., & Torres, V. J. (2014) · Microbiology and Molecular Biology Reviews · doi:10.1128/mmbr.00055-13 · Cited by 276
Prevention and treatment of Staphylococcus aureus biofilms
Bhattacharya, M., Wozniak, D. J., Stoodley, P., & Hall-Stoodley, L. (2015) · Expert Review of Anti-infective Therapy · doi:10.1586/14787210.2015.1100533 · Cited by 265
Metadata
- Authors
- Surewaard, B. G. J., de Haas, C. J. C., Vervoort, F., Rigby, K. M., DeLeo, F. R., Otto, M., van Strijp, J. A. G., & Nijland, R.
- Venue
- Cellular Microbiology
- Publisher
- Hindawi Limited
- Published
- 2013-03-22
- Volume
- 15
- Issue
- 8
- Pages
- 1427-1437
- ISSN
- 1462-5814 (ISSN-L)
- OpenAlex
- W1506145586
- Cited by
- 189
- References
- 11
- FWCI
- 13.24
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: Staphylococcal alpha-phenol soluble modulins contribute to neutrophil lysis after phagocytosis: S. aureus α-PSMs lyse neutrophils from within. https://app.cochat.ai/papers/10.1111/cmi.12130
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- Surewaard, B. G. J., de Haas, C. J. C., Vervoort, F., Rigby, K. M., DeLeo, F. R., Otto, M., van Strijp, J. A. G., & Nijland, R. (2013). Staphylococcal alpha-phenol soluble modulins contribute to neutrophil lysis after phagocytosis: S. aureus α-PSMs lyse neutrophils from within. Cellular Microbiology. https://doi.org/10.1111/cmi.12130
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
