scholarly journals Neutrophil extracellular traps in the host defense against sepsis induced by Burkholderia pseudomallei (melioidosis)

Author(s):  
Hanna K de Jong ◽  
Gavin CKW Koh ◽  
Ahmed Achouiti ◽  
Anne J van der Meer ◽  
Ingrid Bulder ◽  
...  
2012 ◽  
Vol 80 (11) ◽  
pp. 3921-3929 ◽  
Author(s):  
Donporn Riyapa ◽  
Surachat Buddhisa ◽  
Sunee Korbsrisate ◽  
Jon Cuccui ◽  
Brendan W. Wren ◽  
...  

ABSTRACTBurkholderia pseudomalleiis the causative pathogen of melioidosis, of which a major predisposing factor is diabetes mellitus. Polymorphonuclear neutrophils (PMNs) kill microbes extracellularly by the release of neutrophil extracellular traps (NETs). PMNs play a key role in the control of melioidosis, but the involvement of NETs in killing ofB. pseudomalleiremains obscure. Here, we showed that bactericidal NETs were released from human PMNs in response toB. pseudomalleiin a dose- and time-dependent manner.B. pseudomallei-induced NET formation required NADPH oxidase activation but not phosphatidylinositol-3 kinase, mitogen-activated protein kinases, or Src family kinase signaling pathways.B. pseudomalleimutants defective in the virulence-associated Bsa type III protein secretion system (T3SS) or capsular polysaccharide I (CPS-I) induced elevated levels of NETs. NET induction by such mutants was associated with increased bacterial killing, phagocytosis, and oxidative burst by PMNs. Taken together the data imply that T3SS and the capsule may play a role in evading the induction of NETs. Importantly, PMNs from diabetic subjects released NETs at a lower level than PMNs from healthy subjects. Modulation of NET formation may therefore be associated with the pathogenesis and control of melioidosis.


Cells ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 2130
Author(s):  
Shrikant R. Mulay ◽  
Hans-Joachim Anders

Neutrophils are first responders of antimicrobial host defense and sterile inflammation, and therefore, play important roles during health and disease [...]


2016 ◽  
Vol 24 (8) ◽  
pp. 1139-1153 ◽  
Author(s):  
Nardhy Gomez-Lopez ◽  
Roberto Romero ◽  
Yi Xu ◽  
Derek Miller ◽  
Ronald Unkel ◽  
...  

2019 ◽  
Vol 12 (7) ◽  
pp. a037028 ◽  
Author(s):  
Sabrina Sofia Burgener ◽  
Kate Schroder

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hui Wang ◽  
Yiyin Zhang ◽  
Qianling Wang ◽  
Xiaoli Wei ◽  
Hua Wang ◽  
...  

AbstractAs the predominant host defense against pathogens, neutrophil extracellular traps (NETs) have attracted increasing attention due to their vital roles in infectious inflammation in the past few years. Interestingly, NETs also play important roles in noninfectious conditions, such as rheumatism and cancer. The process of NETs formation can be regulated and the form of cell death accompanied by the formation of NETs is regarded as “NETosis”. A large amount of evidence has confirmed that many stimuli can facilitate the release of NETs from neutrophils. Furthermore, it has been illustrated that NETs promote tumor growth and progression via many molecular pathways. Meanwhile, NETs also can promote metastasis in many kinds of cancers based on multiple studies. In addition, some researchs have found that NETs can promote coagulation and cancer-associated thrombosis. In the present review, it will highlight how NETosis, which is stimulated by various stimuli and signaling pathways, affects cancer biological behaviors via NETs. Given their crucial roles in cancer, NETs will become possible therapeutic targets for inhibiting proliferation, metastasis and thrombosis in cancer patients.


2012 ◽  
Vol 12 (1) ◽  
pp. 109-116 ◽  
Author(s):  
Tatsuya Saitoh ◽  
Jun Komano ◽  
Yasunori Saitoh ◽  
Takuma Misawa ◽  
Michihiro Takahama ◽  
...  

Blood ◽  
2019 ◽  
Vol 133 (20) ◽  
pp. 2178-2185 ◽  
Author(s):  
Fernanda V. S. Castanheira ◽  
Paul Kubes

Abstract Neutrophils are an absolutely essential part of the innate immune system, playing an essential role in the control of infectious diseases but more recently are also being viewed as important players in tissue repair. Neutrophils are able to counteract an infection through phagocytosis and/or the release of neutrophil extracellular traps (NETs). By contrast, neutrophils help repair damaged tissues, limiting NET production but still phagocytosing debris. However, when inflammation is recurrent, or the inciting agent persists, neutrophils through a frustrated inability to resolve the problem can release NETs to exacerbate tissue damage during inappropriate inflammation. In this review, we discuss the mechanisms of NET formation, as well as the apparent paradoxical role of neutrophils and NETs in host defense, chronic inflammation, and tissue disrepair.


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