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Infection and Immunity, September 2003, p. 5389-5393, Vol. 71, No. 9
0019-9567/03/$08.00+0 DOI: 10.1128/IAI.71.9.5389-5393.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
Twitching Motility Contributes to the Role of Pili in Corneal Infection Caused by Pseudomonas aeruginosa
Irandokht Zolfaghar,1 David J. Evans,1,2 and Suzanne M. J. Fleiszig1*
School of Optometry, University of California, Berkeley, California 94720,1
Touro University College of Osteopathic Medicine, Vallejo, California 945922
Received 17 March 2003/
Returned for modification 15 April 2003/
Accepted 17 June 2003
Twitching motility is a form of surface-associated bacterial movement mediated by type IV pili of Pseudomonas aeruginosa. Others have shown that pilT and pilU mutants, which are piliated but defective in twitching motility, display reduced cytotoxic capacity towards epithelial cells in vitro. Although these mutants efficiently infected lungs in vivo, they were defective in dissemination to the liver. In this study the role of twitching motility in P. aeruginosa epithelial cell invasion and corneal disease pathogenesis was explored. pilU and pilT mutants of P. aeruginosa strain PAK were compared to a nonpiliated pilA mutant and to wild-type bacteria in their ability to associate with and to invade corneal epithelial cells in vitro and to cause disease in a murine model of corneal infection. As expected, the pilA mutant demonstrated reduced association and invasion of corneal epithelial cells (P < 0.05 in both cases). The pilT mutant, but not the pilU mutant, was less invasive than wild-type PAK was (P < 0.05 versus P = 0.43), while both pilU and pilT mutants exhibited association levels similar to those of the wild type (P = 0.31 and 0.52, respectively). In vivo, all mutants were markedly attenuated in virulence and showed reduced ability to colonize the cornea at 4 and 48 h (all P values < 0.02). Thus, twitching motility contributed to the role of pili in corneal disease but was not involved in the role of pili in adherence to or invasion of corneal epithelial cells.
* Corresponding author. Mailing address: School of Optometry, 688 Minor Hall, University of California, Berkeley, CA 94720-2020. Phone: (510) 643 0990. Fax: (510) 643 5109. E-mail: fleiszig{at}socrates.berkeley.edu.
Editor: D. L. Burns
Infection and Immunity, September 2003, p. 5389-5393, Vol. 71, No. 9
0019-9567/03/$08.00+0 DOI: 10.1128/IAI.71.9.5389-5393.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
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Copyright © 2003 by the American Society for Microbiology. All rights reserved.