C. elegans monitor energy status via the AMPK pathway to trigger innate immune responses against bacterial pathogens.
Journal
Communications biology
ISSN: 2399-3642
Titre abrégé: Commun Biol
Pays: England
ID NLM: 101719179
Informations de publication
Date de publication:
30 06 2022
30 06 2022
Historique:
received:
04
06
2021
accepted:
15
06
2022
entrez:
30
6
2022
pubmed:
1
7
2022
medline:
6
7
2022
Statut:
epublish
Résumé
Pathogen recognition and the triggering of host innate immune system are critical to understanding pathogen-host interaction. Cellular surveillance systems have been identified as an important strategy for the identification of microbial infection. In the present study, using Bacillus thuringiensis-Caenorhabditis elegans as a model, we found an approach for surveillance systems to sense pathogens. We report that Bacillus thuringiensis Cry5Ba, a typical pore-forming toxin, caused mitochondrial damage and energy imbalance by triggering potassium ion leakage, instead of directly targeting mitochondria. Interestingly, we find C. elegans can monitor intracellular energy status to trigger innate immune responses via AMP-activated protein kinase (AMPK), secreting multiple effectors to defend against pathogenic attacks. Our study indicates that the imbalance of energy status is a prevalent side effect of pathogen infection. Furthermore, the AMPK-dependent surveillance system may serve as a practicable strategy for the host to recognize and defense against pathogens.
Identifiants
pubmed: 35773333
doi: 10.1038/s42003-022-03589-1
pii: 10.1038/s42003-022-03589-1
pmc: PMC9246835
doi:
Substances chimiques
Caenorhabditis elegans Proteins
0
AMP-Activated Protein Kinases
EC 2.7.11.31
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
643Subventions
Organisme : NIAID NIH HHS
ID : R01 AI056189
Pays : United States
Organisme : Division of Intramural Research, National Institute of Allergy and Infectious Diseases (Division of Intramural Research of the NIAID)
ID : R01AI056189
Informations de copyright
© 2022. The Author(s).
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