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Pseudomonas aeruginosa adherence to human basement membrane collagen in vitro

University Depts of ¹ Medicine, ² Biochemistry, ³ Diagnostic Radiology and ⁴ Anatomy, Queen Mary Hospital, The University of Hong Kong, Hong Kong SAR, China

CORRESPONDENCE: K.W. Tsang, Division of Respiratory and Critical Care Medicine, University Dept of Medicine, Queen Mary Hospital, The University of Hong Kong, Pokfulam, Hong Kong SAR, China. Fax: 852 28725828. E-mail: kwttsang@hkucc.hku.hk

Keywords: bacterial adherence, basement membrane, collagen, Pseudomonas aeruginosa

Received: October 23, 2002
Accepted January 23, 2003

This study was supported by a research grant from the Hong Kong Research Grants Council, Hong Kong SAR, China.

The mechanisms for Pseudomonas aeruginosa colonisation in the airways of patients with bronchiectasis and cystic fibrosis are poorly understood. P. aeruginosa could evade mucociliary clearance by adhering to the basement membrane at areas denuded of intact respiratory epithelium.

The authors have developed an in vitro model to study P. aeruginosa adherence tohuman basement membrane type-IV collagen by using scanning electron microscopy. P. aeruginosa adherence density was determined as the number of P. aeruginosa per 20microscope fields (2,000x) to log inocular size after incubation at 37°C for 45 min.

The presence of phytohaemagglutinin (PHA)-E, which binds specifically to d-galactose-ß1–4-d-N-acetylglucosamine, significantly reduced P. aeruginosa adherence density compared with control. The presence of heparin and calcium also significantly reduced P. aeruginosa adherence density. P. aeruginosa adherence was not affected by the presence of proline, trans-hydroxyproline, glycine, galactose, N-acetylneuraminic acid, N-acetylglucosamine or Arachis hypogea.

Pseudomonas aeruginosa adherence probably acts via recognition of the d-galactose-ß1–4-d-N-acetylglucosamine sequence on type-IV collagen and this process could be inhibited by heparin and calcium. As persistent Pseudomonas aeruginosa colonisation is detrimental to patients with cystic fibrosis and bronchiectasis and there is currently no effective treatment for its eradication, these results could lead to novel therapy for persistent Pseudomonas aeruginosa infection.

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