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JNK-dependent intestinal barrier failure disrupts host-microbe homeostasis during tumorigenesis

In all animals, the intestinal epithelium forms a tight barrier to the environment. The epithelium regulates the absorption of nutrients, mounts immune responses, and prevents systemic infections. Here, we investigate the consequences of tumorigenesis on the microbiome using a Drosophila intestinal...

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Bibliographic Details
Main Authors: Zhou, Jun (Author) , Boutros, Michael (Author)
Format: Article (Journal)
Language:English
Published: April 10, 2020
In: Proceedings of the National Academy of Sciences of the United States of America
Year: 2020, Volume: 117, Issue: 17, Pages: 9401-9412
ISSN:1091-6490
DOI:10.1073/pnas.1913976117
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1073/pnas.1913976117
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Author Notes:Jun Zhou and Michael Boutros

MARC

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520 |a In all animals, the intestinal epithelium forms a tight barrier to the environment. The epithelium regulates the absorption of nutrients, mounts immune responses, and prevents systemic infections. Here, we investigate the consequences of tumorigenesis on the microbiome using a Drosophila intestinal tumor model. We show that upon loss of BMP signaling, tumors lead to aberrant activation of JNK/Mmp2 signaling, followed by intestinal barrier dysfunction and commensal imbalance. In turn, the dysbiotic microbiome triggers a regenerative response and stimulates tumor growth. We find that inhibiting JNK signaling or depletion of the microbiome restores barrier function of the intestinal epithelium, leading to a reestablishment of host-microbe homeostasis, and organismic lifespan extension. Our experiments identify a JNK-dependent feedback amplification loop between intestinal tumors and the microbiome. They also highlight the importance of controlling the activity level of JNK signaling to maintain epithelial barrier function and host-microbe homeostasis. 
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