Retraction of entero pathogenic E. coli type IV pili promotes efficient host cell colonization, effector translocation and tight junction disruption

Benjamin Aroeti*, Gil Friedman, Efrat Zlotkin-Rivkin, Michael S. Donnenberg

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

23 Scopus citations


Type IV pili (Tfp) play a primary role in mediating the adherence of pathogenic bacteria to their hosts. The pilus filament can retract with an immense force. However, the role of this activity in microbial pathogenesis has not been rigorously explored. Experiments performed on volunteers suggested that the retraction capacity of entero pathogenic Escherichia coli (EPEC) Tfp is required for full virulence. Here we review our recent study1 in which we showed that the retraction capacity of the EPEC Tfp facilitates tight-junction disruption and actin-rich pedestal formation by promoting efficient bacterial protein effector translocation into epithelial host cells. We also present new data using live imaging confocal microscopy suggesting that EPEC adheres to mono layers in micro colonies and that Tfp retraction facilitates significant changes in the micro colony shape, which may be critical for efficient effector delivery. Our studies hence suggest novel insights into the role of pili retraction in EPEC pathogenesis.

Original languageAmerican English
Pages (from-to)267-271
Number of pages5
JournalGut Microbes
Issue number3
StatePublished - 2012

Bibliographical note

Funding Information:
Finally, we have observed that themajority of EPEC microcolonies adhereto polarized monolayers precisely overthe intercellular junctions (Fig. 2). This preferential adherence, reminiscent of the previously noted adherence of enterohemorrhagic E. coli as “log jams” to epithelial junctions,45 does not require the T3SS and is usually the result of initial binding. As EPEC have been demonstrated by numerous investigators1,46-48 to radically alter tight junction function, this observation suggests that EPEC and other enteric pathogens may have evolved a common mechanism to efficiently target this site for maximal effect. Further We are grateful to Ilan Rosenshine, Eitan Zahavi, Naomi Melamed-Book and Joshua A. Lieberman for contributions to the original manuscript. This work was supported in part by Public Health Service Award AI32074 from the National Institutes of Health (M.S.D.) and by the Israel Science Foundation 1167/08 (B.A.).


  • Bundle forming pili
  • Enteropathogenic E. coli
  • Polarized epithelial cells
  • Tight junctions
  • Type IV pili


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