Neonatal imprinting of alveolar macrophages via neutrophil-derived 12-HETE.
Nature
; 614(7948): 530-538, 2023 02.
Article
in English
| MEDLINE | ID: covidwho-2185938
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.
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Macrophages, Alveolar
/
12-Hydroxy-5,8,10,14-eicosatetraenoic Acid
/
Cell Self Renewal
/
Neutrophils
Limits:
Animals
Language:
English
Journal:
Nature
Year:
2023
Document Type:
Article
Affiliation country:
S41586-022-05660-7
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