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C. elegans monitor energy status via the AMPK pathway to trigger innate immune responses against bacterial pathogens
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...
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Published in: | Communications biology 2022-06, Vol.5 (1), p.643-643, Article 643 |
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Main Authors: | , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | 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.
Bacillus thuringiensis
toxin Cry5Ba triggers potassium ion leakage, causing mitochondrial damage and energy imbalance.
C. elegans
can monitor this intracellular energy imbalance via AMP-activated protein kinase to trigger innate immune responses. |
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ISSN: | 2399-3642 2399-3642 |
DOI: | 10.1038/s42003-022-03589-1 |