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Cited by 160

The DOI matches its Crossref record.

Dermatan sulphate is released by proteinases of common pathogenic bacteria and inactivates antibacterial α‐defensin

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Schmidtchen, Artur, Frick, Inga‐Maria, Björck, Lars·2001·Molecular Microbiology
DOI 10.1046/j.1365-2958.2001.02251.x
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Abstract

Defensins represent an evolutionarily conserved group of small peptides with potent antibacterial activities. We report here that extracellular proteinases secreted by the human pathogens Pseudomonas aeruginosa, Enterococcus faecalis and Streptococcus pyogenes release dermatan sulphate by degrading dermatan sulphate‐containing proteoglycans, such as decorin. Dermatan sulphate was found to bind to neutrophil‐derived α‐defensin, and this binding completely neutralized its bactericidal activity. During infection, proteoglycan degradation and release of dermatan sulphate may therefore represent a previously unknown virulence mechanism, which could serve as a target for novel antibacterial strategies.

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Metadata

Authors
Schmidtchen, A., Frick, I., & Björck, L.
Venue
Molecular Microbiology
Publisher
Wiley
Published
2001-02
Volume
39
Issue
3
Pages
708-713
ISSN
  • 0950-382X (ISSN-L)
  • 1365-2958
DOI
10.1046/j.1365-2958.2001.02251.x
OpenAlex
W2024477522
Cited by
160
References
0
FWCI
6.30
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Dermatan sulphate is released by proteinases of common pathogenic bacteria and inactivates antibacterial α‐defensin. https://app.cochat.ai/papers/10.1046/j.1365-2958.2001.02251.x
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Schmidtchen, A., Frick, I., & Björck, L. (2001). Dermatan sulphate is released by proteinases of common pathogenic bacteria and inactivates antibacterial α‐defensin. Molecular Microbiology. https://doi.org/10.1046/j.1365-2958.2001.02251.x

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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.