Lee Kwang-Zin, Lestradet Matthieu, Socha Catherine, Schirmeier Stefanie, Schmitz Antonin, Spenlé Caroline, Lefebvre Olivier, Keime Céline, Yamba Wennida M., Bou Aoun Richard, Liegeois Samuel, Schwab Yannick, Simon-Assmann Patricia, Dalle Frédéric, Ferrandon Dominique
Enterocyte Purge and Rapid Recovery Is a Resilience Reaction of the Gut Epithelium to Pore-Forming Toxin Attack Article de journal
Dans: Cell Host & Microbe, 2016, ISSN: 1931-3128.
Résumé | Liens | BibTeX | Étiquettes: Epithelium, ferrandon, gut, M3i, resilience
@article{Lee2016,
title = {Enterocyte Purge and Rapid Recovery Is a Resilience Reaction of the Gut Epithelium to Pore-Forming Toxin Attack},
author = {Kwang-Zin Lee and Matthieu Lestradet and Catherine Socha and Stefanie Schirmeier and Antonin Schmitz and Caroline Spenlé and Olivier Lefebvre and Céline Keime and Wennida M. Yamba and Richard Bou Aoun and Samuel Liegeois and Yannick Schwab and Patricia Simon-Assmann and Frédéric Dalle and Dominique Ferrandon},
editor = {L Abate},
url = {http://www.sciencedirect.com/science/article/pii/S193131281630436X},
doi = {10.1016/j.chom.2016.10.010},
issn = {1931-3128},
year = {2016},
date = {2016-11-23},
urldate = {2016-11-25},
journal = {Cell Host & Microbe},
abstract = {Summary
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.},
keywords = {Epithelium, ferrandon, gut, M3i, resilience},
pubstate = {published},
tppubtype = {article}
}
Chamy Laure El, Matt Nicolas, Ntwasa Monde, Reichhart Jean-Marc
The multilayered innate immune defense of the gut Article de journal
Dans: Biomed J, vol. 38, no. 4, p. 276–284, 2015, ISSN: 2320-2890.
Résumé | Liens | BibTeX | Étiquettes: fly, gut, innate immunity, M3i, matt, reichhart
@article{el_chamy_multilayered_2015,
title = {The multilayered innate immune defense of the gut},
author = {Laure El Chamy and Nicolas Matt and Monde Ntwasa and Jean-Marc Reichhart},
url = {http://www.biomedj.org/text.asp?2015/38/4/276/158621},
doi = {10.4103/2319-4170.158621},
issn = {2320-2890},
year = {2015},
date = {2015-08-01},
journal = {Biomed J},
volume = {38},
number = {4},
pages = {276--284},
abstract = {In the wild, the fruit fly Drosophila melanogaster thrives on rotten fruit. The digestive tract maintains a powerful gut immune barrier to regulate the ingested microbiota, including entomopathogenic bacteria. This gut immune barrier includes a chitinous peritrophic matrix that isolates the gut contents from the epithelial cells. In addition, the epithelial cells are tightly sealed by septate junctions and can mount an inducible immune response. This local response can be activated by invasive bacteria, or triggered by commensal bacteria in the gut lumen. As with chronic inflammation in mammals, constitutive activation of the gut innate immune response is detrimental to the health of flies. Accordingly, the Drosophila gut innate immune response is tightly regulated to maintain the endogenous microbiota, while preventing infections by pathogenic microorganisms.},
keywords = {fly, gut, innate immunity, M3i, matt, reichhart},
pubstate = {published},
tppubtype = {article}
}