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Neutrophil extracellular traps promote macrophage pyroptosis in sepsis.

Abstract：

:In response to infection, polymorphonuclear neutrophils (PMN) are recruited in the infectious sites, and employ three major strategies to fight against the microbes including phagocytosis, degranulation, and neutrophil extracellular traps (NETs). NETs are a meshwork of chromatin fibers mixed with granule-derived antimicrobial peptides and enzymes, which trap and kill the bacteria extracellularly. In this study, by using a mouse sepsis model, we identified a novel mechanism by which NETs induce macrophage (Mϕ) pyroptosis, a caspase-1-dependent regulated cell death. We show that NET-derived HMGB1, acting through RAGE and dynamin-dependent signaling, triggers an intra-Mϕ cascade of molecular events including cathepsin B (CatB) release from the ruptured lysosomes, followed by pyroptosome formation and caspase-1 activation, and subsequent Mϕ pyroptosis. The study further demonstrates that Mϕ pyroptosis augments inflammatory responses following sepsis. These findings shed light on the proinflammatory role of NETs in mediating PMN-Mϕ interaction, which therefore influences the progress of inflammation following infection.

journal_name

Cell Death Dis

journal_title

Cell death & disease

authors

Chen L,Zhao Y,Lai D,Zhang P,Yang Y,Li Y,Fei K,Jiang G,Fan J

doi

10.1038/s41419-018-0538-5

subject

Has Abstract

pub_date

2018-05-22 00:00:00

pages

597

issue

6

issn

2041-4889

pii

10.1038/s41419-018-0538-5

journal_volume

9

pub_type

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