The Drosophila tumor necrosis factor receptor, Wengen, couples energy expenditure with gut immunity

Research output: Contribution to journal › Journal article › Research › peer-review

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The Drosophila tumor necrosis factor receptor, Wengen, couples energy expenditure with gut immunity. / Loudhaief, Rihab; Jneid, Rouba; Christensen, Christian Fokdal; Mackay, Duncan J; Andersen, Ditte S; Colombani, Julien.

In: Science Advances, Vol. 9, No. 23, eadd4977, 2023.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Loudhaief, R, Jneid, R, Christensen, CF, Mackay, DJ, Andersen, DS & Colombani, J 2023, 'The Drosophila tumor necrosis factor receptor, Wengen, couples energy expenditure with gut immunity', Science Advances, vol. 9, no. 23, eadd4977. https://doi.org/10.1126/sciadv.add4977

APA

Loudhaief, R., Jneid, R., Christensen, C. F., Mackay, D. J., Andersen, D. S., & Colombani, J. (2023). The Drosophila tumor necrosis factor receptor, Wengen, couples energy expenditure with gut immunity. Science Advances, 9(23), [eadd4977]. https://doi.org/10.1126/sciadv.add4977

Vancouver

Loudhaief R, Jneid R, Christensen CF, Mackay DJ, Andersen DS, Colombani J. The Drosophila tumor necrosis factor receptor, Wengen, couples energy expenditure with gut immunity. Science Advances. 2023;9(23). eadd4977. https://doi.org/10.1126/sciadv.add4977

Author

Loudhaief, Rihab ; Jneid, Rouba ; Christensen, Christian Fokdal ; Mackay, Duncan J ; Andersen, Ditte S ; Colombani, Julien. / The Drosophila tumor necrosis factor receptor, Wengen, couples energy expenditure with gut immunity. In: Science Advances. 2023 ; Vol. 9, No. 23.

Bibtex

@article{ca6e216da84c464bb055494638f6ce45,
title = "The Drosophila tumor necrosis factor receptor, Wengen, couples energy expenditure with gut immunity",
abstract = "It is well established that tumor necrosis factor (TNF) plays an instrumental role in orchestrating the metabolic disorders associated with late stages of cancers. However, it is not clear whether TNF/TNF receptor (TNFR) signaling controls energy homeostasis in healthy individuals. Here, we show that the highly conserved Drosophila TNFR, Wengen (Wgn), is required in the enterocytes (ECs) of the adult gut to restrict lipid catabolism, suppress immune activity, and maintain tissue homeostasis. Wgn limits autophagy-dependent lipolysis by restricting cytoplasmic levels of the TNFR effector, TNFR-associated factor 3 (dTRAF3), while it suppresses immune processes through inhibition of the dTAK1/TAK1-Relish/NF-κB pathway in a dTRAF2-dependent manner. Knocking down dTRAF3 or overexpressing dTRAF2 is sufficient to suppress infection-induced lipid depletion and immune activation, respectively, showing that Wgn/TNFR functions as an intersection between metabolism and immunity allowing pathogen-induced metabolic reprogramming to fuel the energetically costly task of combatting an infection.",
author = "Rihab Loudhaief and Rouba Jneid and Christensen, {Christian Fokdal} and Mackay, {Duncan J} and Andersen, {Ditte S} and Julien Colombani",
year = "2023",
doi = "10.1126/sciadv.add4977",
language = "English",
volume = "9",
journal = "Science advances",
issn = "2375-2548",
publisher = "American Association for the Advancement of Science",
number = "23",

}

RIS

TY - JOUR

T1 - The Drosophila tumor necrosis factor receptor, Wengen, couples energy expenditure with gut immunity

AU - Loudhaief, Rihab

AU - Jneid, Rouba

AU - Christensen, Christian Fokdal

AU - Mackay, Duncan J

AU - Andersen, Ditte S

AU - Colombani, Julien

PY - 2023

Y1 - 2023

N2 - It is well established that tumor necrosis factor (TNF) plays an instrumental role in orchestrating the metabolic disorders associated with late stages of cancers. However, it is not clear whether TNF/TNF receptor (TNFR) signaling controls energy homeostasis in healthy individuals. Here, we show that the highly conserved Drosophila TNFR, Wengen (Wgn), is required in the enterocytes (ECs) of the adult gut to restrict lipid catabolism, suppress immune activity, and maintain tissue homeostasis. Wgn limits autophagy-dependent lipolysis by restricting cytoplasmic levels of the TNFR effector, TNFR-associated factor 3 (dTRAF3), while it suppresses immune processes through inhibition of the dTAK1/TAK1-Relish/NF-κB pathway in a dTRAF2-dependent manner. Knocking down dTRAF3 or overexpressing dTRAF2 is sufficient to suppress infection-induced lipid depletion and immune activation, respectively, showing that Wgn/TNFR functions as an intersection between metabolism and immunity allowing pathogen-induced metabolic reprogramming to fuel the energetically costly task of combatting an infection.

AB - It is well established that tumor necrosis factor (TNF) plays an instrumental role in orchestrating the metabolic disorders associated with late stages of cancers. However, it is not clear whether TNF/TNF receptor (TNFR) signaling controls energy homeostasis in healthy individuals. Here, we show that the highly conserved Drosophila TNFR, Wengen (Wgn), is required in the enterocytes (ECs) of the adult gut to restrict lipid catabolism, suppress immune activity, and maintain tissue homeostasis. Wgn limits autophagy-dependent lipolysis by restricting cytoplasmic levels of the TNFR effector, TNFR-associated factor 3 (dTRAF3), while it suppresses immune processes through inhibition of the dTAK1/TAK1-Relish/NF-κB pathway in a dTRAF2-dependent manner. Knocking down dTRAF3 or overexpressing dTRAF2 is sufficient to suppress infection-induced lipid depletion and immune activation, respectively, showing that Wgn/TNFR functions as an intersection between metabolism and immunity allowing pathogen-induced metabolic reprogramming to fuel the energetically costly task of combatting an infection.

U2 - 10.1126/sciadv.add4977

DO - 10.1126/sciadv.add4977

M3 - Journal article

C2 - 37294765

VL - 9

JO - Science advances

JF - Science advances

SN - 2375-2548

IS - 23

M1 - eadd4977

ER -

ID: 355084575