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Bacterial colonization dampens influenza-mediated acute lung injury via induction
of M2 alveolar macrophages
#MMPMID23820884
Wang J
; Li F
; Sun R
; Gao X
; Wei H
; Li LJ
; Tian Z
Nat Commun
2013[]; 4
(?): 2106
PMID23820884
show ga
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.
|Acute Lung Injury/complications/*immunology/*microbiology/pathology/prevention &
control
[MESH]
free
free
free
