scholarly journals Glutathione Reductase Facilitates Host Defense by Sustaining Phagocytic Oxidative Burst and Promoting the Development of Neutrophil Extracellular Traps

2012 ◽  
Vol 188 (5) ◽  
pp. 2316-2327 ◽  
Author(s):  
Jing Yan ◽  
Xiaomei Meng ◽  
Lyn M. Wancket ◽  
Katherine Lintner ◽  
Leif D. Nelin ◽  
...  
Keyword(s):  
Glutathione Reductase ◽  
Host Defense ◽  
Oxidative Burst ◽  
Neutrophil Extracellular Traps ◽  
Extracellular Traps

scholarly journals Neutrophils and Neutrophil Extracellular Traps Regulate Immune Responses in Health and Disease

Cells ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 2130
Author(s):  
Shrikant R. Mulay ◽  
Hans-Joachim Anders
Keyword(s):  
Immune Responses ◽  
Host Defense ◽  
First Responders ◽  
Neutrophil Extracellular Traps ◽  
Sterile Inflammation ◽  
Extracellular Traps ◽  
Health And Disease

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

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

2014 ◽  
Vol 2 (1) ◽  
Author(s):  
Hanna K de Jong ◽  
Gavin CKW Koh ◽  
Ahmed Achouiti ◽  
Anne J van der Meer ◽  
Ingrid Bulder ◽  
...  
Keyword(s):  
Host Defense ◽  
Burkholderia Pseudomallei ◽  
Neutrophil Extracellular Traps ◽  
Extracellular Traps

scholarly journals Neutrophil Extracellular Traps in the Amniotic Cavity of Women with Intra-Amniotic Infection: A New Mechanism of Host Defense

2016 ◽  
Vol 24 (8) ◽  
pp. 1139-1153 ◽  
Author(s):  
Nardhy Gomez-Lopez ◽  
Roberto Romero ◽  
Yi Xu ◽  
Derek Miller ◽  
Ronald Unkel ◽  
...  
Keyword(s):  
Host Defense ◽  
Neutrophil Extracellular Traps ◽  
Amniotic Cavity ◽  
Extracellular Traps

scholarly journals Neutrophil Extracellular Traps in Host Defense

2019 ◽  
Vol 12 (7) ◽  
pp. a037028 ◽  
Author(s):  
Sabrina Sofia Burgener ◽  
Kate Schroder
Keyword(s):  
Host Defense ◽  
Neutrophil Extracellular Traps ◽  
Extracellular Traps

scholarly journals The regulatory mechanism of neutrophil extracellular traps in cancer biological behavior

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hui Wang ◽  
Yiyin Zhang ◽  
Qianling Wang ◽  
Xiaoli Wei ◽  
Hua Wang ◽  
...  
Keyword(s):  
Cell Death ◽  
Host Defense ◽  
Regulatory Mechanism ◽  
Neutrophil Extracellular Traps ◽  
Biological Behavior ◽  
Molecular Pathways ◽  
The Past ◽  
Extracellular Traps ◽  
Promote Tumor Growth ◽  
Cancer Associated Thrombosis

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.

scholarly journals Neutrophil Extracellular Traps Mediate a Host Defense Response to Human Immunodeficiency Virus-1

2012 ◽  
Vol 12 (1) ◽  
pp. 109-116 ◽  
Author(s):  
Tatsuya Saitoh ◽  
Jun Komano ◽  
Yasunori Saitoh ◽  
Takuma Misawa ◽  
Michihiro Takahama ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Host Defense ◽  
Defense Response ◽  
Neutrophil Extracellular Traps ◽  
Extracellular Traps ◽  
Immunodeficiency Virus ◽  
Host Defense Response ◽  
Human Immunodeficiency Virus 1

scholarly journals Neisseria gonorrhoeae Elicits Extracellular Traps in Primary Neutrophil Culture While Suppressing the Oxidative Burst

mBio ◽  
2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Carl W. Gunderson ◽  
H. Steven Seifert
Keyword(s):  
Neisseria Gonorrhoeae ◽  
Oxidative Burst ◽  
Bacterial Species ◽  
Immune Surveillance ◽  
Large Body ◽  
Surface Antigens ◽  
Neutrophil Extracellular Traps ◽  
Content Type ◽  
Extracellular Traps ◽  
Variable Surface

ABSTRACT Neisseria gonorrhoeae(the gonococcus) causes gonorrhea and is uniquely adapted to survive within the human reproductive tract. Gonococci evade host immune surveillance in part by varying their pili and opacity-associated proteins. These variable surface antigens influence interactions with host epithelial and immune cells. A potent polymorphonuclear leukocyte (PMN) response is a hallmark of symptomatic gonococcal infection, with vast numbers of PMNs recruited to the site of infection. A large body of literature describes gonococcus-PMN interactions, but the factors driving the outcome of infection are not fully understood. Gonococci have been described to both induce and suppress the PMN oxidative burst, but we determined that gonococci differentially affect induction of the PMN oxidative burst depending on the multiplicity of infection (MOI). Infecting PMN at an MOI of <20 gonococci elicits an oxidative burst, while an MOI of >20 suppresses the burst. Oxidative burst in response to gonococci is enhanced by, but does not require, expression of pili or opacity proteins. Neutrophil extracellular traps (NETs) were observed in gonococcus-infected PMNs, a process which requires an oxidative burst, yet gonococci induced NETs under suppressing conditions. The NETs were unable to kill gonococci despite killing the common vaginal bacteriumLactobacillus crispatus. Thus, gonococci influence PMN biology to promote their own survival by suppressing the oxidative burst of PMNs and stimulating the formation of NETs, which do not effectively kill gonococci, illustrating how N. gonorrhoeae has evolved to modulate PMN responses to promote infection.IMPORTANCE Neisseria gonorrhoeae, the gonococcus, is the only causative agent of gonorrhea and is exclusively found within the human host. Gonococci stochastically vary the composition of antigens on their surface to evade immune surveillance. We used gonococcal mutants which stably express different surface antigens to dissect interactions between gonococci and primary human polymorphonuclear leukocytes (PMNs). We found that gonococci, depending on the number of bacteria present, either induce or suppress the oxidative burst of PMNs regardless of other stimuli. Gonococci also cause PMNs to release DNA, forming neutrophil extracellular traps (NETs) independently of the oxidative burst. The NETs were unable to kill gonococci but were able to kill commensal bacteria, suggesting that NET production can help gonococci outcompete other bacterial species. We propose that gonococci have evolved to manipulate PMN responses to promote their own survival during infection.

scholarly journals Neutrophils and NETs in modulating acute and chronic inflammation

Blood ◽  
2019 ◽  
Vol 133 (20) ◽  
pp. 2178-2185 ◽  
Author(s):  
Fernanda V. S. Castanheira ◽  
Paul Kubes
Keyword(s):  
Chronic Inflammation ◽  
Host Defense ◽  
Innate Immune System ◽  
Tissue Repair ◽  
Essential Role ◽  
Neutrophil Extracellular Traps ◽  
Innate Immune ◽  
Extracellular Traps ◽  
Acute And Chronic Inflammation

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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