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

Jian Wang, Fengqi Li, Rui Sun, Xiang Gao, Haiming Wei, Lan-Juan Li and Zhigang Tian ()
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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
Xiang Gao: Model Animal Research Center, Nanjing University
Haiming Wei: School of Life Sciences, University of Science and Technology of China
Lan-Juan Li: State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, First Affiliated Hospital, College of Medicine, Zhejiang University
Zhigang Tian: School of Life Sciences, University of Science and Technology of China

Nature Communications, 2013, vol. 4, issue 1, 1-10

Abstract: 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.

Date: 2013
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DOI: 10.1038/ncomms3106

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