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Tissue-Specific Macrophage Responses to Remote Injury Impact the Outcome of Subsequent Local Immune Challenge.

Authors
  • Hoyer, Friedrich Felix1
  • Naxerova, Kamila1
  • Schloss, Maximilian J1
  • Hulsmans, Maarten1
  • Nair, Anil V2
  • Dutta, Partha3
  • Calcagno, David M4
  • Herisson, Fanny1
  • Anzai, Atsushi1
  • Sun, Yuan1
  • Wojtkiewicz, Gregory1
  • Rohde, David1
  • Frodermann, Vanessa1
  • Vandoorne, Katrien1
  • Courties, Gabriel1
  • Iwamoto, Yoshiko1
  • Garris, Christopher S1
  • Williams, David L5
  • Breton, Sylvie2
  • Brown, Dennis2
  • And 7 more
  • 1 Center for Systems Biology, Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, MA 02114, USA.
  • 2 Center for Systems Biology, Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, MA 02114, USA; Program in Membrane Biology and Division of Nephrology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
  • 3 Pittsburgh Heart, Lung, Blood, and Vascular Medicine Institute, Division of Cardiology, Department of Medicine, University of Pittsburgh School of Medicine and University of Pittsburgh Medical Center, BST 1720.1, 200 Lothrop Street, Pittsburgh, PA 15213, USA.
  • 4 Department of Bioengineering, University of California, San Diego, La Jolla, CA 92093, USA.
  • 5 Department of Surgery and Center of Excellence in Inflammation, Infectious Disease and Immunity, East Tennessee State University, 178 Maple Avenue, Johnson City, TN 37614, USA.
  • 6 Neuroscience Center and Department of Pediatrics, Massachusetts General Hospital and Harvard Medical School, Boston, 55 Fruit Street, MA 02114, USA.
  • 7 Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA.
  • 8 Department of Bioengineering, University of California, San Diego, La Jolla, CA 92093, USA; Division of Cardiology, Department of Medicine, University of California San Diego, La Jolla, CA 92093, USA.
  • 9 Center for Systems Biology, Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, MA 02114, USA; Department of Systems Biology, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115, USA.
  • 10 Center for Systems Biology, Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, MA 02114, USA; Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, 185 Cambridge Street, Boston, MA 02114, USA; Department of Internal Medicine I, University Hospital Wuerzburg, Wuerzburg, Germany. Electronic address: [email protected] , (Germany)
Type
Published Article
Journal
Immunity
Publication Date
Nov 19, 2019
Volume
51
Issue
5
Identifiers
DOI: 10.1016/j.immuni.2019.10.010
PMID: 31732166
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Myocardial infarction, stroke, and sepsis trigger systemic inflammation and organism-wide complications that are difficult to manage. Here, we examined the contribution of macrophages residing in vital organs to the systemic response after these injuries. We generated a comprehensive catalog of changes in macrophage number, origin, and gene expression in the heart, brain, liver, kidney, and lung of mice with myocardial infarction, stroke, or sepsis. Predominantly fueled by heightened local proliferation, tissue macrophage numbers increased systemically. Macrophages in the same organ responded similarly to different injuries by altering expression of tissue-specific gene sets. Preceding myocardial infarction improved survival of subsequent pneumonia due to enhanced bacterial clearance, which was caused by IFNɣ priming of alveolar macrophages. Conversely, EGF receptor signaling in macrophages exacerbated inflammatory lung injury. Our data suggest that local injury activates macrophages in remote organs and that targeting macrophages could improve resilience against systemic complications following myocardial infarction, stroke, and sepsis. Copyright © 2019 Elsevier Inc. All rights reserved.

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