P75NTR+CD64+ neutrophils promote sepsis-induced acute lung injury

Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 263(2024) vom: 01. Juni, Seite 110206
1. Verfasser: Fu, Di (VerfasserIn)
Weitere Verfasser: Gao, Shan, Li, Jia-Nan, Cui, Yan-Hui, Luo, Yan-Wei, Zhong, Yan-Jun, Li, Qiao, Luo, Cong, Dai, Ru-Ping, Luo, Ru-Yi, Hu, Zhao-Lan
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2024
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article CD64(+) neutrophils Phagocytosis Sepsis-induced acute lung injury p75(NTR) Ngfr protein, mouse NGFR protein, human
Beschreibung
Zusammenfassung:Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.
Patients suffering from sepsis-induced acute lung injury (ALI) exhibit a high mortality rate, and their prognosis is closely associated with infiltration of neutrophils into the lungs. In this study, we found a significant elevation of CD64+ neutrophils, which highly expressed p75 neurotrophin receptor (p75NTR) in peripheral blood of mice and patients with sepsis-induced ALI. p75NTR+CD64+ neutrophils were also abundantly expressed in the lung of ALI mice induced by lipopolysaccharide. Conditional knock-out of the myeloid lineage's p75NTR gene improved the survival rates, attenuated lung tissue inflammation, reduced neutrophil infiltration and enhanced the phagocytic functions of CD64+ neutrophils. In vitro, p75NTR+CD64+ neutrophils exhibited an upregulation and compromised phagocytic activity in blood samples of ALI patients. Blocking p75NTR activity by soluble p75NTR extracellular domain peptide (p75ECD-Fc) boosted CD64+ neutrophils phagocytic activity and reduced inflammatory cytokine production via regulation of the NF-κB activity. The findings strongly indicate that p75NTR+CD64+ neutrophils are a novel pathogenic neutrophil subpopulation promoting sepsis-induced ALI
Beschreibung:Date Completed 17.05.2024
Date Revised 22.08.2024
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2024.110206