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Akoumianaki T, Vaporidi K, Diamantaki E, et al. Uncoupling of IL-6 signaling and LC3-associated phagocytosis drives immunoparalysis during sepsis. Cell Host Microbe. 2021;29(8):1277-1293.e6doi: 10.1016/j.chom.2021.06.002.
Akoumianaki, T., Vaporidi, K., Diamantaki, E., Pène, F., Beau, R., Gresnigt, M. S., Gkountzinopulou, M., Venichaki, M., Drakos, E., El-Benna, J., Samonis, G., Le, K. T. T., Kumar, V., Georgopoulos, D., van de Veerdonk, F. L., Netea, M. G., Latge, J. P., & Chamilos, G. (2021). Uncoupling of IL-6 signaling and LC3-associated phagocytosis drives immunoparalysis during sepsis. Cell host & microbe, 29(8), 1277-1293.e6. https://doi.org/10.1016/j.chom.2021.06.002
Akoumianaki, Tonia, et al. "Uncoupling of IL-6 signaling and LC3-associated phagocytosis drives immunoparalysis during sepsis." Cell host & microbe vol. 29,8 (2021): 1277-1293.e6. doi: https://doi.org/10.1016/j.chom.2021.06.002
Akoumianaki T, Vaporidi K, Diamantaki E, Pène F, Beau R, Gresnigt MS, Gkountzinopulou M, Venichaki M, Drakos E, El-Benna J, Samonis G, Le KTT, Kumar V, Georgopoulos D, van de Veerdonk FL, Netea MG, Latge JP, Chamilos G. Uncoupling of IL-6 signaling and LC3-associated phagocytosis drives immunoparalysis during sepsis. Cell Host Microbe. 2021 Aug 11;29(8):1277-1293.e6. doi: 10.1016/j.chom.2021.06.002. Epub 2021 Jul 01. PMID: 34214493.
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Cell Host Microbe. 2021 Aug 11;29(8):1277-1293.e6. doi: 10.1016/j.chom.2021.06.002. Epub 2021 Jul 01.

Uncoupling of IL-6 signaling and LC3-associated phagocytosis drives immunoparalysis during sepsis.

Cell host & microbe

Tonia Akoumianaki, Katerina Vaporidi, Eleni Diamantaki, Frédéric Pène, Remi Beau, Mark S Gresnigt, Marina Gkountzinopulou, Maria Venichaki, Elias Drakos, Jamel El-Benna, George Samonis, Kieu T T Le, Vinod Kumar, Dimitrios Georgopoulos, Frank L van de Veerdonk, Mihai G Netea, Jean-Paul Latge, Georgios Chamilos

Affiliations

  1. Laboratory of Clinical Microbiology and Microbial Pathogenesis, School of Medicine, University of Crete, Voutes, 71110 Heraklion, Crete, Greece.
  2. Department of Intensive Care Medicine, University Hospital of Heraklion, School of Medicine, University of Crete, Voutes, 71110 Heraklion, Crete, Greece.
  3. Medical ICU, Hôpital Cochin, Hôpitaux Universitaires Paris Centre, Assistance Publique - Hôpitaux de Paris, Institut Cochin INSERM U1016, CNRS UMR 8104, Université Paris Descartes, Paris, France.
  4. Unité des Aspergillus, Institut Pasteur, Paris 75015, France.
  5. Department of Internal Medicine (463) and Radboud Center for Infectious Diseases (RCI), Radboudumc, Geert Grooteplein 8, 6500 HB Nijmegen, the Netherlands; Department of Microbial Pathogenicity Mechanisms, Leibniz Institute for Natural Product Research and Infection Biology - Hans-Knoell-Institute, Beutenbergstrasse 11a, 07745 Jena, Germany.
  6. Laboratory of Clinical Chemistry, School of Medicine, University of Crete, Voutes, 71110 Heraklion, Crete, Greece.
  7. Department of Pathology, School of Medicine, University of Crete, Voutes, 71110 Heraklion, Crete, Greece.
  8. Université de Paris, Centre de Recherche sur l'Inflammation (CRI), INSERM U1149, CNRS-ERL 8252, Laboratoire d'Excellence Inflamex, Faculté de Médecine Xavier Bichat, Paris, France.
  9. Department of Internal Medicine (463) and Radboud Center for Infectious Diseases (RCI), Radboudumc, Geert Grooteplein 8, 6500 HB Nijmegen, the Netherlands; University of Groningen, University Medical Center Groningen, Department of Genetics, Groningen, the Netherlands.
  10. Department of Internal Medicine (463) and Radboud Center for Infectious Diseases (RCI), Radboudumc, Geert Grooteplein 8, 6500 HB Nijmegen, the Netherlands.
  11. Department of Internal Medicine (463) and Radboud Center for Infectious Diseases (RCI), Radboudumc, Geert Grooteplein 8, 6500 HB Nijmegen, the Netherlands; Department for Genomics & Immunoregulation, Life and Medical Sciences Institute (LIMES), University of Bonn, 53115 Bonn, Germany.
  12. Laboratory of Clinical Microbiology and Microbial Pathogenesis, School of Medicine, University of Crete, Voutes, 71110 Heraklion, Crete, Greece; Unité des Aspergillus, Institut Pasteur, Paris 75015, France.
  13. Laboratory of Clinical Microbiology and Microbial Pathogenesis, School of Medicine, University of Crete, Voutes, 71110 Heraklion, Crete, Greece; Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology, 71300 Heraklion, Crete, Greece. Electronic address: [email protected].

PMID: 34214493 DOI: 10.1016/j.chom.2021.06.002

Abstract

Immune deactivation of phagocytes is a central event in the pathogenesis of sepsis. Herein, we identify a master regulatory role of IL-6 signaling on LC3-associated phagocytosis (LAP) and reveal that uncoupling of these two processes during sepsis induces immunoparalysis in monocytes/macrophages. In particular, we demonstrate that activation of LAP by the human fungal pathogen Aspergillus fumigatus depends on ERK1/2-mediated phosphorylation of p47phox subunit of NADPH oxidase. Physiologically, autocrine IL-6/JAK2/Ninein axis orchestrates microtubule organization and dynamics regulating ERK recruitment to the phagosome and LC3

Copyright © 2021 Elsevier Inc. All rights reserved.

Keywords: Aspergillus fumigatus; IL-6; JAK; LAP; LC3-associated phagocytosis; NADPH oxidase; extracellular-signal-kinase regulated (ERK); microtubules; phagosome; sepsis; sepsis immunoparalysis

Conflict of interest statement

Declaration of interests The authors declare no competing interests.

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