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Thromb Haemost 2004; 92(02): 281-287
DOI: 10.1160/TH03-12-0732
Theme Issue Article
Schattauer GmbH

Heparin binding protein is increased in chronic leg ulcer fluid and released from granulocytes by secreted products of Pseudomonas aeruginosa

Katarina Lundqvist
1   Section for Dermatology, Department of Medical Microbiology, Dermatology and Infection, Lund University, Biomedical Center, Lund, Sweden
,
Heiko Herwald
2   Section for Molecular Pathogenesis, Department of Cell and Molecular Biology, Lund University, Biomedical Center, Lund, Sweden
,
Andreas Sonesson
1   Section for Dermatology, Department of Medical Microbiology, Dermatology and Infection, Lund University, Biomedical Center, Lund, Sweden
,
Artur Schmidtchen
1   Section for Dermatology, Department of Medical Microbiology, Dermatology and Infection, Lund University, Biomedical Center, Lund, Sweden
› Institutsangaben
Financial support: This work was supported by grants from the Swedish Medical Research Council (projects 13471), the Royal Physiographic Society in Lund, the Welander-Finsen, Magnus Bergvall, Crafoord, Alfred Österlund, Groschinsky, Åhlen, Lundgren, Lion and Kock Foundations, and Mölnlycke Health Care AB.
Weitere Informationen

Publikationsverlauf

Received 02. Dezember 2003

Accepted after revision 30. März 2004

Publikationsdatum:
30. November 2017 (online)

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Summary

Recently it was demonstrated by Gautam, et al. that release of neutrophil-borne heparin-binding protein (HBP), also known as CAP37/azurocidin, induced endothelial hyperpermeability and neutrophil efflux. Here, we show that chronic leg ulcer fluid, in contrast to wound fluid from acute wounds, contains highly increased levels of HBP. Immunohistochemistry demonstrated the presence of HBP in chronic ulcer tissues. Furthermore, secreted products of Pseudomonas aeruginosa were found to induce release of HBP from human neutrophils. Our data suggest a possible link between bacterial presence and HBPrelease in chronic ulcers.Thus, targeting HBP offers an interesting option for reduction of endothelial barrier dysfunction in chronic ulcers.

Keywords

Wound healing - inflammation - skin - blood - aprotinin
 

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