scholarly journals Diminished neutrophil extracellular trap (NET) formation is a novel innate immune deficiency induced by acute ethanol exposure in polymicrobial sepsis, which can be rescued by CXCL1

2017 ◽  
Vol 13 (9) ◽  
pp. e1006637 ◽  
Author(s):  
Liliang Jin ◽  
Sanjay Batra ◽  
Samithamby Jeyaseelan
Aging Cell ◽  
2014 ◽  
Vol 13 (4) ◽  
pp. 690-698 ◽  
Author(s):  
Jon Hazeldine ◽  
Phillipa Harris ◽  
Iain L. Chapple ◽  
Melissa Grant ◽  
Hannah Greenwood ◽  
...  

2015 ◽  
Vol 7 (5) ◽  
pp. 459-465 ◽  
Author(s):  
Lieke A. Golbach ◽  
Marleen H. Scheer ◽  
Jan J.M. Cuppen ◽  
Huub Savelkoul ◽  
B.M. Lidy Verburg-van Kemenade

Low-frequency (LF) electromagnetic fields (EMFs) are abundantly present in modern society, and the potential biological consequences of exposure to these fields are under intense debate. Immune cells are suggested as possible target cells, though a clear mechanism is lacking. Considering their crucial role in innate immune activation, we selected an ex vivo exposure set-up with human neutrophils to investigate a possible correlation between neutrophil extracellular trap (NET) formation and LF EMF exposure. Our study shows that formation of NETs is enhanced by LF EMF exposure. Enhanced NET formation leads to increased antimicrobial properties as well as damage to surrounding cells. We found that LF-EMF-induced NET formation is dependent on the NADPH oxidase pathway and production of reactive oxygen species. Additionally, LF EMF exposure does not influence autophagy and PAD4 activity. Our study provides a mechanism by which exposure to LF EMFs could influence the innate immune system.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Qian Ou ◽  
Jia-qi Fang ◽  
Zhe-sheng Zhang ◽  
Zhe Chi ◽  
Jie Fang ◽  
...  

AbstractTcpC is a multifunctional virulence factor of uropathogenic E. coli (UPEC). Neutrophil extracellular trap formation (NETosis) is a crucial anti-infection mechanism of neutrophils. Here we show the influence of TcpC on NETosis and related mechanisms. We show NETosis in the context of a pyelonephritis mouse model induced by TcpC-secreting wild-type E. coli CFT073 (CFT073wt) and LPS-induced in vitro NETosis with CFT073wt or recombinant TcpC (rTcpC)-treated neutrophils are inhibited. rTcpC enters neutrophils through caveolin-mediated endocytosis and inhibits LPS-induced production of ROS, proinflammatory cytokines and protein but not mRNA levels of peptidylarginine deiminase 4 (PAD4). rTcpC treatment enhances PAD4 ubiquitination and accumulation in proteasomes. Moreover, in vitro ubiquitination kit analyses show that TcpC is a PAD4-targetd E3 ubiquitin-ligase. These data suggest that TcpC inhibits NETosis primarily by serving as an E3 ligase that promotes degradation of PAD4. Our findings provide a novel mechanism underlying TcpC-mediated innate immune evasion.


2020 ◽  
Vol 131 ◽  
pp. 110497
Author(s):  
Bárbara Osmarin Turra ◽  
Fernanda Barbisan ◽  
Verônica Farina Azzolin ◽  
Cibele Ferreira Teixeira ◽  
Thamara Flores ◽  
...  

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