Enterocyte Purge and Rapid Recovery Is a Resilience Reaction of the Gut Epithelium to Pore-Forming Toxin Attack

Publication date: Available online 23 November 2016
Source:Cell Host & Microbe
Author(s): Kwang-Zin Lee, Matthieu Lestradet, Catherine Socha, Stefanie Schirmeier, Antonin Schmitz, Caroline Spenlé, Olivier Lefebvre, Céline Keime, Wennida M. Yamba, Richard Bou Aoun, Samuel Liegeois, Yannick Schwab, Patricia Simon-Assmann, Frédéric Dalle, Dominique Ferrandon
Besides digesting nutrients, the gut protects the host against invasion by pathogens. Enterocytes may be subjected to damage by both microbial and host defensive responses, causing their death. Here, we report a rapid epithelial response that alleviates infection stress and protects the enterocytes from the action of microbial virulence factors. Intestinal epithelia exposed to hemolysin, a pore-forming toxin secreted by Serratia marcescens, undergo an evolutionarily conserved process of thinning followed by the recovery of their initial thickness within a few hours. In response to hemolysin attack, Drosophila melanogaster enterocytes extrude most of their apical cytoplasm, including damaged organelles such as mitochondria, yet do not lyse. We identify two secreted peptides, the expression of which requires CyclinJ, that mediate the recovery phase in which enterocytes regain their original shape and volume. Epithelial thinning and recovery constitute a fast and efficient response to intestinal infections, with pore-forming toxins acting as alarm signals.

Graphical abstract

Teaser

Bacterial pore-forming toxins damage host cells. Lee, Lestradet et al. find that enterocytes exposed to these toxins extrude much of their apical cytoplasm, purging themselves of damaged components and bacteria. The thinned epithelium recovers its original shape within hours via a process that requires CyclinJ-dependent signaling between enterocytes.


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