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Research Article

Diabetes Exacerbates Infection via Hyperinflammation by Signaling through TLR4 and RAGE

Travis B. Nielsen, Paul Pantapalangkoor, Jun Yan, Brian M. Luna, Ken Dekitani, Kevin Bruhn, Brandon Tan, Justin Junus, Robert A. Bonomo, Ann Marie Schmidt, Michael Everson, Frederick Duncanson, Terence M. Doherty, Lin Lin, Brad Spellberg
Paul Dunman, Editor
Travis B. Nielsen
Department of Medicine and Department of Molecular Microbiology and Immunology, Keck School of Medicine at the University of Southern California (USC), Los Angeles, California, USA
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Paul Pantapalangkoor
Department of Medicine and Department of Molecular Microbiology and Immunology, Keck School of Medicine at the University of Southern California (USC), Los Angeles, California, USA
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Jun Yan
Department of Medicine and Department of Molecular Microbiology and Immunology, Keck School of Medicine at the University of Southern California (USC), Los Angeles, California, USA
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Brian M. Luna
Department of Medicine and Department of Molecular Microbiology and Immunology, Keck School of Medicine at the University of Southern California (USC), Los Angeles, California, USA
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Ken Dekitani
Department of Medicine and Department of Molecular Microbiology and Immunology, Keck School of Medicine at the University of Southern California (USC), Los Angeles, California, USA
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Kevin Bruhn
Department of Medicine and Department of Molecular Microbiology and Immunology, Keck School of Medicine at the University of Southern California (USC), Los Angeles, California, USA
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Brandon Tan
Department of Medicine and Department of Molecular Microbiology and Immunology, Keck School of Medicine at the University of Southern California (USC), Los Angeles, California, USA
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Justin Junus
Department of Medicine and Department of Molecular Microbiology and Immunology, Keck School of Medicine at the University of Southern California (USC), Los Angeles, California, USA
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Robert A. Bonomo
Departments of Medicine, Pharmacology and Molecular Biology and Microbiology, Louis Stokes Cleveland Department of Veterans Affairs Medical Center, Case Western Reserve University, Cleveland, Ohio, USA
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Ann Marie Schmidt
Departments of Medicine, Biochemistry and Molecular Pharmacology and Pathology, New York University, New York, New York, USA
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Michael Everson
Eisai, Inc., Tokyo, Japan
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Frederick Duncanson
Eisai, Inc., Tokyo, Japan
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Terence M. Doherty
Los Angeles Biomedical Research Institute, Torrance, California, USA
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Lin Lin
Los Angeles Biomedical Research Institute, Torrance, California, USA
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Brad Spellberg
Department of Medicine and Department of Molecular Microbiology and Immunology, Keck School of Medicine at the University of Southern California (USC), Los Angeles, California, USA
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Paul Dunman
University of Rochester
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DOI: 10.1128/mBio.00818-17
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Article Information

DOI 
https://doi.org/10.1128/mBio.00818-17
PubMed 
28830942

Published By 
American Society for Microbiology
History 
  • Received May 15, 2017
  • Accepted July 6, 2017
  • Published online August 22, 2017.

Copyright & Usage 
This is a work of the U.S. Government and is not subject to copyright protection in the United States. Foreign copyrights may apply.
Editors and / or Reviewers 
  • Paul Dunman, Editor, University of Rochester

Author Information

  1. Travis B. Nielsena,
  2. Paul Pantapalangkoora,
  3. Jun Yana,
  4. Brian M. Lunaa,
  5. Ken Dekitania,
  6. Kevin Bruhna,
  7. Brandon Tana,
  8. Justin Junusa,
  9. Robert A. Bonomob,
  10. Ann Marie Schmidtc,
  11. Michael Eversond,
  12. Frederick Duncansond,
  13. Terence M. Dohertye,
  14. Lin Line,
  15. Brad Spellberga
  1. aDepartment of Medicine and Department of Molecular Microbiology and Immunology, Keck School of Medicine at the University of Southern California (USC), Los Angeles, California, USA
  2. bDepartments of Medicine, Pharmacology and Molecular Biology and Microbiology, Louis Stokes Cleveland Department of Veterans Affairs Medical Center, Case Western Reserve University, Cleveland, Ohio, USA
  3. cDepartments of Medicine, Biochemistry and Molecular Pharmacology and Pathology, New York University, New York, New York, USA
  4. dEisai, Inc., Tokyo, Japan
  5. eLos Angeles Biomedical Research Institute, Torrance, California, USA
  • Address correspondence to Travis B. Nielsen, travis.nielsen{at}gmail.com.
  • Citation Nielsen TB, Pantapalangkoor P, Yan J, Luna BM, Dekitani K, Bruhn K, Tan B, Junus J, Bonomo RA, Schmidt AM, Everson M, Duncanson F, Doherty TM, Lin L, Spellberg B. 2017. Diabetes exacerbates infection via hyperinflammation by signaling through TLR4 and RAGE. mBio 8:e00818-17. https://doi.org/10.1128/mBio.00818-17.

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Diabetes Exacerbates Infection via Hyperinflammation by Signaling through TLR4 and RAGE
Travis B. Nielsen, Paul Pantapalangkoor, Jun Yan, Brian M. Luna, Ken Dekitani, Kevin Bruhn, Brandon Tan, Justin Junus, Robert A. Bonomo, Ann Marie Schmidt, Michael Everson, Frederick Duncanson, Terence M. Doherty, Lin Lin, Brad Spellberg
mBio Aug 2017, 8 (4) e00818-17; DOI: 10.1128/mBio.00818-17

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Diabetes Exacerbates Infection via Hyperinflammation by Signaling through TLR4 and RAGE
Travis B. Nielsen, Paul Pantapalangkoor, Jun Yan, Brian M. Luna, Ken Dekitani, Kevin Bruhn, Brandon Tan, Justin Junus, Robert A. Bonomo, Ann Marie Schmidt, Michael Everson, Frederick Duncanson, Terence M. Doherty, Lin Lin, Brad Spellberg
mBio Aug 2017, 8 (4) e00818-17; DOI: 10.1128/mBio.00818-17
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KEYWORDS

diabetes mellitus
Gram-negative bacteria
infection
inflammation
RAGE
TLR4

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