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

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, Shradha Wali, Renaud Prevel, Jun Ding, James G. Martin, Ajitha Thanabalasuriar, Bryan G. Yipp, Luis B. Barreiro and Maziar Divangahi ()
Additional contact information
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
Maziar Divangahi: Meakins-Christie Laboratories, McGill University

Nature, 2023, vol. 614, issue 7948, 530-538

Abstract: 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.

Date: 2023
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DOI: 10.1038/s41586-022-05660-7

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