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Pseudomonas aeruginosa internalization by corneal epithelial cells involves MEK and ERK signal transduction proteins

  1. David J Evans1,2,
  2. Inna A Maltseva1,
  3. Josephine Wu1,
  4. Suzanne M.J Fleiszig1,*

Article first published online: 9 JAN 2006

DOI: 10.1111/j.1574-6968.2002.tb11288.x

Issue

FEMS Microbiology Letters

FEMS Microbiology Letters

Volume 213, Issue 1, pages 73–79, July 2002

Additional Information

How to Cite

Evans, D. J., Maltseva, I. A., Wu, J. and Fleiszig, S. M.J. (2002), Pseudomonas aeruginosa internalization by corneal epithelial cells involves MEK and ERK signal transduction proteins. FEMS Microbiology Letters, 213: 73–79. doi: 10.1111/j.1574-6968.2002.tb11288.x

Author Information

  1. 1

    Morton D. Sarver Laboratory for Cornea and Contact Lens Research, School of Optometry, University of California, Berkeley, CA 94720, USA

  2. 2

    Touro University College of Osteopathic Medicine, Vallejo, CA 94592, USA

* *Corresponding author. Tel.: +1 (510) 643 0990; Fax: +1 (510) 643 5109, E-mail address: fleiszig@socrates.berkeley.edu

Publication History

  1. Issue published online: 9 JAN 2006
  2. Article first published online: 9 JAN 2006
  3. Received 14 May 2002, Accepted 23 May 2002

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Keywords:

  • Pseudomonas aeruginosa;
  • Invasion;
  • Epithelium;
  • Mitogen-activated protein kinase;
  • Cornea

Abstract

Invasion of epithelial cells represents a potential pathogenic mechanism for Pseudomonas aeruginosa. We explored the role of mitogen-activated protein kinase kinases (MEK 1/2) and the extracellular signal-regulated kinases (ERK 1/2) in P. aeruginosa invasion. Treatment of corneal epithelial cells with MEK inhibitors, PD98059 (20 μM) or UO126 (100 μM), reduced P. aeruginosa invasion by ∼60% without affecting bacterial association with the cells (P=0.0001). UO124, a negative control for UO126, had no effect on bacterial internalization. Infection of cells with an internalization-defective flhA mutant of P. aeruginosa was associated with less ERK 1/2 tyrosine phosphorylation than infection with wild-type invasive P. aeruginosa. An ERK-2 inhibitor, 5-iodotubercidin (20 μM), reduced P. aeruginosa invasion by ∼40% (P=0.035). Together, these data suggest that P. aeruginosa internalization by epithelial cells involves a pathway(s) that includes MEK and ERK signaling proteins.

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