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Neonatal imprinting of alveolar macrophages via neutrophil-derived 12-HETE

Author

Listed:
  • Erwan Pernet

    (Meakins-Christie Laboratories, McGill University)

  • Sarah Sun

    (University of Chicago)

  • Nicole Sarden

    (University of Calgary)

  • Saideep Gona

    (University of Chicago)

  • Angela Nguyen

    (University of Calgary)

  • Nargis Khan

    (Meakins-Christie Laboratories, McGill University)

  • Martin Mawhinney

    (McGill University)

  • Kim A. Tran

    (Meakins-Christie Laboratories, McGill University)

  • Julia Chronopoulos

    (Meakins-Christie Laboratories, McGill University)

  • Dnyandeo Amberkar

    (Meakins-Christie Laboratories, McGill University)

  • Mina Sadeghi

    (McGill University)

  • Alexandre Grant

    (McGill University)

  • Shradha Wali

    (Meakins-Christie Laboratories, McGill University)

  • Renaud Prevel

    (Meakins-Christie Laboratories, McGill University)

  • Jun Ding

    (Meakins-Christie Laboratories, McGill University)

  • James G. Martin

    (Meakins-Christie Laboratories, McGill University)

  • Ajitha Thanabalasuriar

    (McGill University)

  • Bryan G. Yipp

    (University of Calgary)

  • Luis B. Barreiro

    (University of Chicago
    CHU Sainte-Justine Research Center)

  • Maziar Divangahi

    (Meakins-Christie Laboratories, McGill University
    McGill University
    McGill University
    McGill University)

Abstract

Resident-tissue macrophages (RTMs) arise from embryonic precursors1,2, yet the developmental signals that shape their longevity remain largely unknown. Here we demonstrate in mice genetically deficient in 12-lipoxygenase and 15-lipoxygenase (Alox15−/− mice) that neonatal neutrophil-derived 12-HETE is required for self-renewal and maintenance of alveolar macrophages (AMs) during lung development. Although the seeding and differentiation of AM progenitors remained intact, the absence of 12-HETE led to a significant reduction in AMs in adult lungs and enhanced senescence owing to increased prostaglandin E2 production. A compromised AM compartment resulted in increased susceptibility to acute lung injury induced by lipopolysaccharide and to pulmonary infections with influenza A virus or SARS-CoV-2. Our results highlight the complexity of prenatal RTM programming and reveal their dependency on in trans eicosanoid production by neutrophils for lifelong self-renewal.

Suggested Citation

  • Erwan Pernet & Sarah Sun & Nicole Sarden & Saideep Gona & Angela Nguyen & Nargis Khan & Martin Mawhinney & Kim A. Tran & Julia Chronopoulos & Dnyandeo Amberkar & Mina Sadeghi & Alexandre Grant & Shrad, 2023. "Neonatal imprinting of alveolar macrophages via neutrophil-derived 12-HETE," Nature, Nature, vol. 614(7948), pages 530-538, February.
    • Handle: RePEc:nat:nature:v:614:y:2023:i:7948:d:10.1038_s41586-022-05660-7
    DOI: 10.1038/s41586-022-05660-7
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