TLR signalling augments macrophage bactericidal activity through mitochondrial ROS

A. Phillip West, Igor E. Brodsky, Christoph Rahner, Dong Kyun Woo, Hediye Erdjument-Bromage, Paul Tempst, Matthew C. Walsh, Yongwon Choi, Gerald S. Shadel and Sankar Ghosh ()
Additional contact information
A. Phillip West: Yale University School of Medicine
Igor E. Brodsky: Yale University School of Medicine
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

Nature, 2011, vol. 472, issue 7344, 476-480

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.

Date: 2011
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DOI: 10.1038/nature09973

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