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Neutrophil pyroptosis mediates pathology of P. aeruginosa lung infection in the absence of the NADPH oxidase NOX2

Authors
 J-C Ryu  ;  M-J Kim  ;  Y Kwon  ;  J-H Oh  ;  SS Yoon  ;  SJ Shin  ;  J-H Yoon  ;  J-H Ryu 
Citation
 MUCOSAL IMMUNOLOGY, Vol.10(3) : 757-774, 2017 
Journal Title
MUCOSAL IMMUNOLOGY
ISSN
 1933-0219 
Issue Date
2017
MeSH
Animals ; Apoptosis* ; Apoptosis Regulatory Proteins/genetics ; Calcium-Binding Proteins/genetics ; Flagellin/metabolism ; Humans ; Immunocompromised Host ; Inflammasomes/metabolism* ; Lung/immunology* ; Lung/microbiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; NADPH Oxidase 2/genetics ; NADPH Oxidase 2/metabolism* ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; Neutrophils/immunology* ; Neutrophils/microbiology ; Pseudomonas Infections/immunology* ; Pseudomonas aeruginosa/immunology* ; Toll-Like Receptor 5/genetics
Abstract
Nod-like receptor family, CARD domain-containing 4 (NLRC4) inflammasome activation is required for efficient clearance of intracellular pathogens through caspsase-1-dependent pyroptosis in macrophages. Although neutrophils have a critical role in protection from Pseudomonas aeruginosa infection, the mechanisms regulating inflammasome-mediated pyroptosis in neutrophils and its physiological role are largely unknown. We sought to determine the specific mechanisms regulating neutrophil pyroptosis in P. aeruginosa strain PAO1 (PAO1) lung infection and to identify the pathological role of this process. Nox2-/- models with reduced neutrophil antibacterial activity exhibited increased neutrophil pyroptosis, which was mediated by flagellin, a pathogenic PAO1 component. We also demonstrate that PAO1-induced pyroptosis depended on NLRC4 and Toll-like receptor 5 (TLR5) in neutrophils generated from Nlrc4-/- or Tlr5-/- mice. Our study reveals previously unknown mechanisms and physiological role of neutrophil pyroptosis during P. aeruginosa lung infection. Furthermore, our findings regarding neutrophil pyroptosis in the context of neutrophil dysfunction may explain the causes of acute and/or chronic infectious diseases discovered in immune-compromised patients.
Full Text
https://www.nature.com/mi/journal/v10/n3/full/mi201673a.html
DOI
10.1038/mi.2016.73
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Otorhinolaryngology (이비인후과학교실) > 1. Journal Papers
Yonsei Authors
Ryu, Jae Chan(류재찬)
Ryu, Ji Hwan(유지환)
Yoon, Sang Sun(윤상선) ORCID logo https://orcid.org/0000-0003-2979-365X
Yoon, Joo Heon(윤주헌)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/153549
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