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Infection and Immunity, October 2003, p. 5565-5575, Vol. 71, No. 10
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.10.5565-5575.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Mucin Degradation Mechanisms by Distinct Pseudomonas aeruginosa Isolates In Vitro

Lina Panayiota Aristoteli^* and Mark D. P. Willcox

Cooperative Research Centre for Eye Research and Technology, University of New South Wales, Sydney 2052, Australia

Received 20 February 2003/ Returned for modification 28 May 2003/ Accepted 13 July 2003

Pseudomonas aeruginosa has emerged as an important causative agent of bacterial keratitis, a rapidly progressive ocular condition that may result in blindness. Secretory mucin forms the main constituent of the precorneal tear film, a three-layer film on the ocular surface protecting the underlying corneal epithelium from potential pathogens. The purpose of the present study was to compare mucin degradation mechanisms between ocular P. aeruginosa strains. Mucin degradation was assessed by agarose electrophoresis, lectin blotting, and size exclusion chromatography. The results indicate that certain P. aeruginosa strains (Paer12, ATCC 15442, 6294, and Paer25) had depleted mucin from the culture supernatant and that this was contingent on the inherent ability of these isolates to produce proteases. Non-protease-producing strains (Paer1 and Paer3) did not appreciably degrade mucin. Further, galactosidase, N-acetylglucosaminidase, and N-acetylgalactosaminidase activities were detected in some strains, suggesting the operation of further mechanisms of mucin degradation by P. aeruginosa. Mucin degradation by P. aeruginosa also seemed to be for the acquisition of nutrients, as a growth advantage was observed in mucin-depleting strains over nondepleting strains in the long term. It is postulated that the degradation of mucin serves to collapse the mucin barrier and its associated network containing antibacterial tear components and to provide energy for sustained bacterial growth.

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* Corresponding author. Present address: Heart Research Institute, 145-147 Missenden Rd., Camperdown, Sydney 2050, Australia. Phone: 61 2 9550 3560. Fax: 61 2 9550 3302. E-mail: l.aristoteli{at}hri.org.au.

Editor: J. D. Clements

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Infection and Immunity, October 2003, p. 5565-5575, Vol. 71, No. 10
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.10.5565-5575.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

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