IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v4y2013i1d10.1038_ncomms3106.html
   My bibliography  Save this article

Bacterial colonization dampens influenza-mediated acute lung injury via induction of M2 alveolar macrophages

Author

Listed:
  • Jian Wang

    (School of Life Sciences, University of Science and Technology of China)

  • Fengqi Li

    (School of Life Sciences, University of Science and Technology of China)

  • Rui Sun

    (School of Life Sciences, University of Science and Technology of China
    Hefei National Laboratory for Physical Sciences at Microscale)

  • Xiang Gao

    (Model Animal Research Center, Nanjing University)

  • Haiming Wei

    (School of Life Sciences, University of Science and Technology of China
    Hefei National Laboratory for Physical Sciences at Microscale)

  • Lan-Juan Li

    (State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, First Affiliated Hospital, College of Medicine, Zhejiang University
    Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases)

  • Zhigang Tian

    (School of Life Sciences, University of Science and Technology of China
    Hefei National Laboratory for Physical Sciences at Microscale
    State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, First Affiliated Hospital, College of Medicine, Zhejiang University
    Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases)

Abstract

While the presence of airway bacteria is known to be associated with improved immunity against influenza virus, the mechanism by which endogenous microbiota influence antiviral immunity remains unclear. Here we show that specific pathogen-free mice are more sensitive to influenza-mediated death than mice living in a natural environment. Priming with Toll-like receptor 2-ligand+ Staphylococcus aureus, which commonly colonizes the upper respiratory mucosa, significantly attenuates influenza-mediated lung immune injury. Toll-like receptor 2 deficiency or alveolar macrophage depletion abolishes this protection. S. aureus priming recruits peripheral CCR2+CD11b+ monocytes into the alveoli that polarize to M2 alveolar macrophages in an environment created by Toll-like receptor 2 signalling. M2 alveolar macrophages inhibit influenza-mediated lethal inflammation via anti-inflammatory cytokines and inhibitory ligands. Our results suggest a previously undescribed mechanism by which the airway microbiota may protect against influenza-mediated lethal inflammation.

Suggested Citation

  • Jian Wang & Fengqi Li & Rui Sun & Xiang Gao & Haiming Wei & Lan-Juan Li & Zhigang Tian, 2013. "Bacterial colonization dampens influenza-mediated acute lung injury via induction of M2 alveolar macrophages," Nature Communications, Nature, vol. 4(1), pages 1-10, October.
    • Handle: RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms3106
    DOI: 10.1038/ncomms3106
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms3106
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/ncomms3106?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms3106. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.