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2023
Huang Jianqiong, Lou Yanyan, Liu Jiyong, Bulet Philippe, Cai Chuping, Ma Kaiyu, Jiao Renjie, Hoffmann Jules A, Liégeois Samuel, Lia Zi, Ferrandon Dominique
A Toll pathway effector protects Drosophila specifically from distinct toxins secreted by a fungus or a bacterium Journal Article
In: PNAS, vol. 120, no. 12, 2023.
Abstract | Links | BibTeX | Tags: Baramicin A, Destruxin A, disease tolerance, enterocin O16, ferrandon, hoffmann, M3i, microbial toxins, resilience
@article{Huang2023,
title = {A Toll pathway effector protects Drosophila specifically from distinct toxins secreted by a fungus or a bacterium},
author = {Jianqiong Huang and Yanyan Lou and Jiyong Liu and Philippe Bulet and Chuping Cai and Kaiyu Ma and Renjie Jiao and Jules A Hoffmann and Samuel Liégeois and Zi Lia and Dominique Ferrandon},
editor = {Hugo Bellen, Baylor College of Medicine, Houston, TX},
url = {https://doi.org/10.1073/pnas.2205140120},
doi = {10.1073/pnas.2205140120},
year = {2023},
date = {2023-03-14},
urldate = {2023-03-14},
journal = {PNAS},
volume = {120},
number = {12},
abstract = {Major immune response pathways control the expression of hundreds of genes that represent potential effectors of the immune response. The Drosophila Toll pathway is required in the host defenses against several Gram-positive bacterial infections as well as against fungal infections. The current paradigm is that peptides secreted in the hemolymph during the systemic immune response are either bona fide antimicrobial peptides or likely ones. The finding of a dual role for one Toll pathway effector in the resilience to both Enterococcus faecalis and Metarhizium robertsii infections underscores an original concept in insect innate immunity. Evolution can select effectors tailored to protect the host from the action of microbial toxins of prokaryotic or eukaryotic origin, independently of antibodies or detoxification pathways.},
keywords = {Baramicin A, Destruxin A, disease tolerance, enterocin O16, ferrandon, hoffmann, M3i, microbial toxins, resilience},
pubstate = {published},
tppubtype = {article}
}
Major immune response pathways control the expression of hundreds of genes that represent potential effectors of the immune response. The Drosophila Toll pathway is required in the host defenses against several Gram-positive bacterial infections as well as against fungal infections. The current paradigm is that peptides secreted in the hemolymph during the systemic immune response are either bona fide antimicrobial peptides or likely ones. The finding of a dual role for one Toll pathway effector in the resilience to both Enterococcus faecalis and Metarhizium robertsii infections underscores an original concept in insect innate immunity. Evolution can select effectors tailored to protect the host from the action of microbial toxins of prokaryotic or eukaryotic origin, independently of antibodies or detoxification pathways.
2016
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 Journal Article
In: Cell Host & Microbe, 2016, ISSN: 1931-3128.
Abstract | Links | BibTeX | Tags: 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}
}
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.
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.
