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

Cell Host Microbe. 2016 Dec 14;20(6):716-730. doi: 10.1016/j.chom.2016.10.010. Epub 2016 Nov 23.


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.

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Bacterial Toxins / toxicity*
  • Cell Death / drug effects
  • Cytoplasm / drug effects
  • Digestive System / drug effects*
  • Digestive System / immunology
  • Digestive System / microbiology
  • Digestive System / pathology
  • Disease Models, Animal
  • Drosophila melanogaster
  • Enterocytes / drug effects*
  • Enterocytes / metabolism*
  • Enterocytes / pathology
  • Hemolysin Proteins / metabolism
  • Hemolysin Proteins / toxicity
  • Intestinal Diseases / microbiology
  • Intestinal Mucosa / drug effects*
  • Intestinal Mucosa / immunology
  • Intestinal Mucosa / metabolism*
  • Intestinal Mucosa / pathology
  • Microvilli / drug effects
  • Mitochondria / drug effects
  • Serratia Infections
  • Serratia marcescens / metabolism
  • Serratia marcescens / pathogenicity
  • Survival
  • Varroidae
  • Virulence Factors


  • Bacterial Toxins
  • Hemolysin Proteins
  • Virulence Factors