Abstract

The Neisseria gonorrhoeae type IV pilus is a retractile appendage that can generate forces near 100 pN. We tested the hypothesis that type IV pilus retraction influences epithelial cell gene expression by exerting tension on the host membrane. Wild-type and retraction-defective bacteria altered the expression of an identical set of epithelial cell genes during attachment. Interestingly, pilus retraction, per se, did not regulate novel gene expression but, rather, enhanced the expression of a subset of the infection-regulated genes. This is accomplished through mitogen-activated protein kinase activation and at least one other undefined stress-activated pathway. These results can be reproduced by applying artificial force on the epithelial membrane, using a magnet and magnetic beads. Importantly, this retraction-mediated signaling increases the ability of the cell to withstand apoptotic signals triggered by infection. We conclude that pilus retraction stimulates mechanosensitive pathways that enhance the expression of stress-responsive genes and activate cytoprotective signaling. A model for the role of pilus retraction in influencing host cell survival is presented.

Highlights

  • Many pathogenic and nonpathogenic bacteria produce type IV pili (Tfp), among them, Neisseria gonorrhoeae, N. meningitidis, Pseudomonas aeruginosa, Legionella pneumophila, enteropathogenic and enterohemorrhagic Escherichia coli, and Vibrio cholerae [1]

  • To segregate the genes responding to pilus retraction, a wt to pilT fold-change expression ratio (W/P) was calculated for each infection-regulated gene

  • We examined mitogen-activated protein kinase (MAPK) phosphorylation in T84 cells infected with N400pilT to determine whether kinase activation was influenced by pilus retraction

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Summary

Introduction

Many pathogenic and nonpathogenic bacteria produce type IV pili (Tfp), among them, Neisseria gonorrhoeae, N. meningitidis, Pseudomonas aeruginosa, Legionella pneumophila, enteropathogenic and enterohemorrhagic Escherichia coli, and Vibrio cholerae [1]. Tfp are fimbriate organelles that play a crucial role in the interaction of the bacterium with its environment, as evidenced by their requirement for motility [2], biofilm formation [3,4], and horizontal gene transfer [5,6,7]. These appendages promote bacterial attachment to host cells and contribute to virulence [8,9,10,11,12].

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