Elastase-producing Pseudomonas aeruginosa degrade plasma proteins and extracellular products of human skin and fibroblasts, and inhibit fibroblast growth.

Abstract

Leg ulcers of venous origin represent a disease affecting 0.1-0.2% of the population. It is known that almost all chronic ulcers are colonized by different bacteria, such as staphylococci, enterococci and Pseudomonas aeruginosa. We here report that P. aeruginosa, expressing the major metalloproteinase elastase, induces degradation of complement C3, various antiproteinases, kininogens, fibroblast proteins, and proteoglycans (PG) in vitro, thus mimicking proteolytic activity previously identified in chronic ulcer fluid in vivo. Elastase-producing P. aeruginosa isolates were shown to significantly degrade human wound fluid as well as human skin proteins ex vivo. Elastase-containing conditioned P. aeruginosa medium and purified elastase inhibited fibroblast cell growth. These effects, in conjunction with the finding that proteinase production was detected in wound fluid ex vivo, suggest that bacterial proteinases play a pathogenic role in chronic ulcers.

• Authors: Artur Schmidtchen, Elisabet Holst, Hans Tapper, Lars Björck
• Journal: Microbial pathogenesis (Microb Pathog) Vol. 34 Issue 1 Pg. 47-55 (Jan 2003) ISSN: 0882-4010 [Print] England
• PMID: 12620384 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Bacterial Proteins
• Blood Proteins
• Complement C3
• Culture Media, Conditioned
• Extracellular Matrix Proteins
• Kininogens
• Protease Inhibitors
• Proteoglycans
• Metalloendopeptidases
• pseudolysin, Pseudomonas aeruginosa
• serralysin

Topics

• Apoptosis (drug effects)
• Bacterial Proteins (genetics, metabolism, pharmacology)
• Blood Proteins (metabolism)
• Body Fluids (microbiology)
• Cell Division (drug effects)
• Chronic Disease
• Cloning, Molecular
• Complement C3 (metabolism)
• Culture Media, Conditioned (pharmacology)
• Extracellular Matrix Proteins (metabolism)
• Female
• Fibroblasts (drug effects, metabolism)
• Genes, Bacterial
• Humans
• Kininogens (metabolism)
• Leg Ulcer (etiology, microbiology)
• Mastectomy
• Metalloendopeptidases (genetics, metabolism, pharmacology)
• Protease Inhibitors (metabolism)
• Proteoglycans (metabolism)
• Pseudomonas Infections (microbiology)
• Pseudomonas aeruginosa (enzymology, genetics, isolation & purification)
• Skin (cytology, metabolism)
• Surgical Wound Infection (microbiology)
• Venous Insufficiency (complications)