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

被引：25

作者：

Pernet, Erwan ^{[1
]}

Sun, Sarah ^{[2
]}

Sarden, Nicole ^{[3
]}

Gona, Saideep ^{[2
]}

Nguyen, Angela ^{[3
]}

Khan, Nargis ^{[1
]}

Mawhinney, Martin ^{[4
]}

Tran, Kim A. ^{[1
]}

Chronopoulos, Julia ^{[1
]}

Amberkar, Dnyandeo ^{[1
]}

Sadeghi, Mina ^{[5
]}

Grant, Alexandre ^{[5
]}

Wali, Shradha ^{[1
]}

Prevel, Renaud ^{[1
]}

Ding, Jun ^{[1
]}

Martin, James G. ^{[1
]}

Thanabalasuriar, Ajitha ^{[4
]}

Yipp, Bryan G. ^{[3
]}

Barreiro, Luis B. ^{[2
,6
]}

Divangahi, Maziar ^{[1
,5
,7
,8
]}

机构：

[1] McGill Univ, McGill Univ Hlth Ctr, Meakins Christie Labs, Montreal, PQ, Canada

[2] Univ Chicago, Dept Med, Sect Genet Med, Chicago, IL USA

[3] Univ Calgary, Phoebe & Joan Snyder Inst Chron Dis, Cumming Sch Med, Dept Crit Care, Calgary, AB, Canada

[4] McGill Univ, Dept Pharmacol & Therapeut, Montreal, PQ, Canada

[5] McGill Univ, Dept Microbiol & Immunol, Montreal, PQ, Canada

[6] CHU Sainte Justine Res Ctr, Dept Genet, Montreal, PQ, Canada

[7] McGill Univ, Dept Pathol, Montreal, PQ, Canada

[8] McGill Univ, McGill Int TB Ctr, Montreal, PQ, Canada

来源：

NATURE | 2023年 / 614卷 / 7948期

关键词：

ALLERGIC INFLAMMATION; EICOSANOID PATHWAYS; PROSTAGLANDIN E-2; FETAL MONOCYTES; INFLUENZA-VIRUS; I INTERFERON; SENESCENCE; PROMOTES; IMMUNITY; LUNG;

D O I：

10.1038/s41586-022-05660-7

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Resident-tissue macrophages (RTMs) arise from embryonic precursors(1,2), 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 E-2 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.

引用

页码：530 / +

页数：35

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[1] HTSeq-a Python']Python framework to work with high-throughput sequencing data [J].