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

Katarina Lundqvist; Heiko Herwald; Andreas Sonesson; Artur Schmidtchen

doi:10.1160/TH03-12-0732

Thrombosis and Haemostasis, Table of Contents

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

¹Section for Dermatology, Department of Medical Microbiology, Dermatology and Infection, Lund University, Biomedical Center, Lund, Sweden

,

Heiko Herwald

²Section for Molecular Pathogenesis, Department of Cell and Molecular Biology, Lund University, Biomedical Center, Lund, Sweden

,

Andreas Sonesson

¹Section for Dermatology, Department of Medical Microbiology, Dermatology and Infection, Lund University, Biomedical Center, Lund, Sweden

,

Artur Schmidtchen

¹Section for Dermatology, Department of Medical Microbiology, Dermatology and Infection, Lund University, Biomedical Center, Lund, Sweden

› Author Affiliations

Abstract

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

Full Text

References

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