Journal
NATURE IMMUNOLOGY
Volume 21, Issue 2, Pages 145-+Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41590-019-0568-x
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Funding
- Francis Crick Institute
- Cancer Research UK [FC001206]
- UK Medical Research Council [FC001206]
- Wellcome Trust [FC001206]
- MRC [U117597139]
- BBSRC-GSK-funded case studentship [BB/L502315/1]
- MRC [MC_U117597139] Funding Source: UKRI
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Respiratory infections occur throughout life but how this shapes the lung immune system through time is unclear. Wack and colleagues show that a previous influenza infection recruits monocytes to the lung, which then assume an alveolar macrophage-like phenotype and mediate long-term antibacterial protection. Despite the prevalence and clinical importance of influenza, its long-term effect on lung immunity is unclear. Here we describe that following viral clearance and clinical recovery, at 1 month after infection with influenza, mice are better protected from Streptococcus pneumoniae infection due to a population of monocyte-derived alveolar macrophages (AMs) that produce increased interleukin-6. Influenza-induced monocyte-derived AMs have a surface phenotype similar to resident AMs but display a unique functional, transcriptional and epigenetic profile that is distinct from resident AMs. In contrast, influenza-experienced resident AMs remain largely similar to naive AMs. Thus, influenza changes the composition of the AM population to provide prolonged antibacterial protection. Monocyte-derived AMs persist over time but lose their protective profile. Our results help to understand how transient respiratory infections, a common occurrence in human life, can constantly alter lung immunity by contributing monocyte-derived, recruited cells to the AM population.
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