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TLR signalling augments macrophage bactericidal activity through mitochondrial ROS

Author

Listed:
  • A. Phillip West

    (Yale University School of Medicine)

  • Igor E. Brodsky

    (Yale University School of Medicine
    Present address: Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, Pennsylvania 19104, USA.)

  • Christoph Rahner

    (Yale University School of Medicine)

  • Dong Kyun Woo

    (Yale University School of Medicine)

  • Hediye Erdjument-Bromage

    (Molecular Biology Program, Memorial Sloan-Kettering Cancer Center)

  • Paul Tempst

    (Molecular Biology Program, Memorial Sloan-Kettering Cancer Center)

  • Matthew C. Walsh

    (University of Pennsylvania School of Medicine)

  • Yongwon Choi

    (University of Pennsylvania School of Medicine)

  • Gerald S. Shadel

    (Yale University School of Medicine)

  • Sankar Ghosh

    (College of Physicians and Surgeons, Columbia University)

Abstract

Mitochondrial role in innate immunity The stimulation of a subset of surface Toll-like receptors (TLRs), transmembrane proteins of the innate immune system that recognize microbe-derived molecules, is shown to induce production of reactive oxygen for bacterial killing by the mitochondrial pathway. When the 'bacterial' TLRs (TLR1, 2 and 4) bind to a ligand they promote the recruitment of mitochondria to macrophage phagosomes and induce upregulation of mitochondrial reactive oxygen species (mROS). This work implicates mROS as important components of antibacterial responses and further establishes mitochondria as hubs for innate immune signalling.

Suggested Citation

  • A. Phillip West & Igor E. Brodsky & Christoph Rahner & Dong Kyun Woo & Hediye Erdjument-Bromage & Paul Tempst & Matthew C. Walsh & Yongwon Choi & Gerald S. Shadel & Sankar Ghosh, 2011. "TLR signalling augments macrophage bactericidal activity through mitochondrial ROS," Nature, Nature, vol. 472(7344), pages 476-480, April.
    • Handle: RePEc:nat:nature:v:472:y:2011:i:7344:d:10.1038_nature09973
    DOI: 10.1038/nature09973
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    Cited by:

    1. Sanghyeon Choi & Youngjin Lee & Shinhye Park & Song Yee Jang & Jongbin Park & Do Won Oh & Su-Man Kim & Tae-Hwan Kim & Ga Seul Lee & Changyi Cho & Byoung Sik Kim & Donghan Lee & Eun-Hee Kim & Hae-Kap C, 2024. "Dissemination of pathogenic bacteria is reinforced by a MARTX toxin effector duet," Nature Communications, Nature, vol. 15(1), pages 1-20, December.
    2. Xudong Wang & Siyu Su & Yuqing Zhu & Xiaolong Cheng & Chen Cheng & Leilei Chen & Anhua Lei & Li Zhang & Yuyan Xu & Dan Ye & Yi Zhang & Wei Li & Jin Zhang, 2023. "Metabolic Reprogramming via ACOD1 depletion enhances function of human induced pluripotent stem cell-derived CAR-macrophages in solid tumors," Nature Communications, Nature, vol. 14(1), pages 1-15, December.
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    5. Jawaher Alharthi & Ali Bayoumi & Khaled Thabet & Ziyan Pan & Brian S. Gloss & Olivier Latchoumanin & Mischa Lundberg & Natalie A. Twine & Duncan McLeod & Shafi Alenizi & Leon A. Adams & Martin Weltman, 2022. "A metabolic associated fatty liver disease risk variant in MBOAT7 regulates toll like receptor induced outcomes," Nature Communications, Nature, vol. 13(1), pages 1-19, December.
    6. Clive Drakeford & Sonia Aguila & Fiona Roche & Karsten Hokamp & Judicael Fazavana & Mariana P. Cervantes & Annie M. Curtis & Heike C. Hawerkamp & Sukhraj Pal Singh Dhami & Hugo Charles-Messance & Emer, 2022. "von Willebrand factor links primary hemostasis to innate immunity," Nature Communications, Nature, vol. 13(1), pages 1-19, December.
    7. Shuai Gao & Lingyu Gao & Dailin Yuan & Xu’ai Lin & Stijn Veen, 2024. "Gonococcal OMV-delivered PorB induces epithelial cell mitophagy," Nature Communications, Nature, vol. 15(1), pages 1-15, December.
    8. Lulu Ren & Jianqin Wan & Xiaoyan Li & Jie Yao & Yan Ma & Fanchao Meng & Shusen Zheng & Weidong Han & Hangxiang Wang, 2024. "Mitochondrial rewiring with small-molecule drug-free nanoassemblies unleashes anticancer immunity," Nature Communications, Nature, vol. 15(1), pages 1-20, December.

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