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1 ation of a barricade comprised of neutrophil extracellular traps.
2 city was not due to resistance to neutrophil extracellular traps.
3 roduction of highly prothrombotic neutrophil extracellular traps.
4 required to trigger formation of neutrophil extracellular traps.
5 tissues and areas that displayed neutrophil extracellular traps.
6 d can also block the formation of neutrophil extracellular traps.
7 of their nuclear contents to form neutrophil extracellular traps.
8 irulence factors and formation of neutrophil extracellular traps.
9 g by human neutrophils and within neutrophil extracellular traps.
10 icroparticles, cell-free DNA, and neutrophil extracellular traps.
11 ng phagocytosis and generation of neutrophil extracellular traps.
12 ine receptor CXCR4 and to release neutrophil extracellular traps.
13 9 on activated human PMN surfaces and in PMN extracellular traps; 2) minimal immunoreactive and activ
14 as revealed with the discovery of neutrophil extracellular traps, a specialized cell death process in
15 zyme important for the release of neutrophil extracellular traps, abolished neutrophil aggregation an
16 itro, with release of extensive histone-rich extracellular traps, an event unsuppressed by dexamethas
17 DNase I to root tips eliminates border cell extracellular traps and abolishes root tip resistance to
18 ial killing, trigger formation of neutrophil extracellular traps and appear to partake in inflammatio
19 e the major protein components of neutrophil extracellular traps and are known to have cytotoxic effe
22 killing by neutrophils and within neutrophil extracellular traps and neutralizes LL-37 chemotactic pr
23 ized' neutrophils, as well as the neutrophil extracellular traps and other products made by neutrophi
24 trate of PAD4, localize H1 within neutrophil extracellular traps, and detect autoantibodies to citrul
25 ses mtDNA release, IFN signaling, neutrophil extracellular traps, and disease severity in a mouse mod
26 is or necrosis, degranulation, or release of extracellular traps, and it decreases the oxidative resp
27 pture exogenous material, extrude neutrophil extracellular traps, and kill bacteria via cathelicidin
28 w players, such as polyphosphate, neutrophil extracellular traps, and microparticles, which have been
29 n, decreases bacterial killing by neutrophil extracellular traps, and modulates S. pyogenes virulence
30 d reactive oxygen species, escape neutrophil extracellular traps, and promote and accelerate phagocyt
31 d lysis, engulfment, formation of neutrophil extracellular traps, and release of antimicrobial peptid
32 nomic DNA, mitochondrial DNA, and neutrophil extracellular traps, and shuttles them in the cytosol of
34 FN by pDCs, which were induced by neutrophil extracellular traps arising from the endocytosis of the
36 an increase in the deployment of neutrophil extracellular traps associated with hyperglycemia slows
37 ng, kidney, and heart, containing neutrophil extracellular traps associated with platelets and fibrin
42 in type 2 CRSwNP, associated with eosinophil extracellular traps cell death and Charcot-Leyden crysta
44 ophils were less prone to undergo neutrophil extracellular traps cell death in the tissue of patients
45 MCs with Leishmania led to generation of MC extracellular traps comprising of DNA, histones and tryp
50 ntal model of asthma would induce eosinophil extracellular traps (EETs) in bronchoalveolar lavage flu
51 eractions induce the formation of eosinophil extracellular traps (EETs), which are present in human t
54 e mechanism is reminiscent of the neutrophil extracellular traps (ETs) recently described in vertebra
55 o their unique ability to release neutrophil extracellular traps even in the absence of pathogens.
56 We previously demonstrated that neutrophil extracellular traps exacerbate pulmonary injury during i
58 ng biofilms, where they underwent neutrophil extracellular trap formation (NETosis) in response to hi
59 type IV), an enzyme essential for neutrophil extracellular trap formation (NETosis), is released toge
61 yeloid cell recruitment, and more neutrophil extracellular trap formation (NETs) in WT compared to pc
62 plasmatic coagulation but induced neutrophil extracellular trap formation and DNA release mainly from
64 mechanism that is associated with neutrophil extracellular trap formation and selective autophagy in
66 in transgenic mice with impaired neutrophil extracellular trap formation and/or neutrophils with con
67 exhibited an elevated capacity in neutrophil extracellular trap formation at baseline and upon microb
68 Thus, initial characterization of macrophage extracellular trap formation due to M. tuberculosis infe
69 ing bacteria and an impairment of neutrophil extracellular trap formation in vivo during KPn pneumoni
70 yeloid cells, but did not require neutrophil extracellular trap formation involving peptidyl arginine
72 otein 78, and reduced spontaneous neutrophil extracellular trap formation of bone marrow-derived neut
73 phaMbeta2 integrin activation and neutrophil extracellular trap formation under inflammatory conditio
74 lling and were fully competent in neutrophil extracellular trap formation, a recently identified extr
75 severe pulmonary edema, increased neutrophil extracellular trap formation, and elevated concentration
76 ne-induced neutrophil congestion, neutrophil extracellular trap formation, and thrombosis in the pulm
77 ing, oxidative burst, chemotaxis, neutrophil extracellular trap formation, bacterial killing, and ind
78 essels does not require fibrin generation or extracellular trap formation, but involves GPIbalpha-vWF
79 y increased leukocyte engagement, neutrophil extracellular trap formation, fibrin, and local activati
80 siding macrophages, potentiate foam cell and extracellular trap formation, induce endothelial dysfunc
81 nce of ESX-1, IFN-gamma does not restore any extracellular trap formation, mycobacterial aggregation,
82 ulitis and controls, and assessed neutrophil extracellular trap formation, reactive oxygen species pr
83 led to a significant reduction in neutrophil extracellular trap formation, reactive oxygen species pr
90 severe disease display excessive neutrophil extracellular traps formation, neutrophil-inflammation a
91 bulins from ANCA(+) sputum allowed extensive extracellular trap formations from both neutrophils and
92 eveloped computational pipelines to identify extracellular traps from an in vitro human samples visua
94 ate cell activation that included neutrophil extracellular trap generation and elevated surface expre
95 ponse, and we present evidence of neutrophil extracellular trap generation during experimental urinar
96 n or inhibition of the release of neutrophil extracellular traps had little effects, but platelet P2Y
97 n in RA, their ability to extrude neutrophil extracellular traps has recently been implicated in the
100 fungal filaments, suggesting that neutrophil extracellular traps help to protect the epithelial barri
102 nt findings of the involvement of neutrophil extracellular traps in atherogenesis and atherothrombosi
103 d by limited tools to quantify occurrence of extracellular traps in experimental models and human sam
104 demonstrate the importance of neutrophil extracellular traps in helminth damage after primary inf
105 ng/mL; p </= 0.05) and identified neutrophil extracellular traps in kidney and liver tissues from unt
109 at model, we identified layers of neutrophil extracellular traps interconnecting and entrapping bacte
110 es to its advantage by converting neutrophil extracellular traps into a bacterial weapon against macr
112 ation and membrane pore formation, and (iii) extracellular trapping mediated by membrane-proximal hep
113 to counteract histone as well as neutrophil extracellular trap-mediated cytotoxicity against host ce
114 ate proteoglycan(s) is present in neutrophil extracellular traps, modulates histone affinity, and mod
115 a fulminant and self-propagating neutrophil extracellular trap (NET) and cytokine response, but inde
117 t evidence suggests that enhanced neutrophil extracellular trap (NET) formation activates plasmacytoi
118 o immobilized neutrophils induced neutrophil extracellular trap (NET) formation in response to infect
120 e immune infiltration with robust neutrophil extracellular trap (NET) formation in the skeletal muscl
121 ice) result in type I IFN-induced neutrophil extracellular trap (NET) formation that promotes bacteri
122 on of IL-4 receptor subunits, (2) neutrophil extracellular trap (NET) formation, (3) migration toward
123 active oxygen species production, neutrophil extracellular trap (NET) formation, and neutrophil elast
124 h neutrophil functions, including neutrophil extracellular trap (NET) formation, are involved in the
132 is, oxidative burst capacity, and neutrophil extracellular trap (NET) generation (NETosis) were measu
133 After the recent description of neutrophil extracellular trap (NET) release by activated neutrophil
135 granule proteins with subsequent neutrophil extracellular trap (NET) release independent of elastase
137 Neutrophil responses, including neutrophil extracellular trap (NET) release, were intact in endothe
138 We previously showed that anti-neutrophil extracellular trap (NET) rheumatoid arthritis (RA)-rmAbs
139 and host components that included neutrophil extracellular trap (NET) structures and that the bacteri
144 trophil complexes, a signature of neutrophil extracellular traps (NET), in the kidneys of tumor-beari
146 tosis and cell death by releasing neutrophil extracellular traps (NETs) (NETosis), which were more ob
148 These chromatin traps are termed neutrophil extracellular traps (NETs) and are decorated with granul
149 o contributes to the formation of neutrophil extracellular traps (NETS) and impacts on the immune res
150 ophils exposed to S. aureus biofilms produce extracellular traps (NETs) and phagocytose bacteria, bot
151 -1 mediates bacterial survival in neutrophil extracellular traps (NETs) and protects GAS from antimic
152 ivation of leukocytes, release of neutrophil extracellular traps (NETs) and severe inflammation.
153 report a pathogenic link between neutrophil extracellular traps (NETs) and the formation of gallston
154 activation, and the formation of neutrophil extracellular traps (NETs) and to elucidate the signalin
163 ale: Extracellular DNA (eDNA) and neutrophil extracellular traps (NETs) are implicated in multiple in
167 ygen species (ROS) and release of neutrophil extracellular traps (NETs) by activated neutrophils are
168 eir anti-microbial defense, neutrophils form extracellular traps (NETs) by releasing decondensed chro
172 crucial role in sepsis, releasing neutrophil extracellular traps (NETs) composed of DNA complexed wit
180 We also studied the production of neutrophil extracellular traps (NETs) from single neutrophils isola
185 illebrand factor) and presence of neutrophil extracellular traps (NETs) have been implicated in liver
189 e particles induce the release of neutrophil extracellular traps (NETs) in a size-dependent manner by
190 Here, we report the presence of neutrophil extracellular traps (NETs) in cardiac tissue of patients
192 reactive oxygen species (ROS) and neutrophil extracellular traps (NETs) in mouse and human neutrophil
194 obe size and selectively released neutrophil extracellular traps (NETs) in response to large pathogen
195 tient were incapable of producing neutrophil extracellular traps (NETs) in response to ROS and were u
196 trophils release large amounts of neutrophil extracellular traps (NETs) in the presence of P. aerugin
199 cies in the phagosome and release neutrophil extracellular traps (NETs) into their surroundings to im
201 tes and the possible formation of neutrophil extracellular traps (NETs) may result in chromatin relea
203 but neutrophil products including neutrophil extracellular traps (NETs) mediate host organ damage and
204 itates formation of prothrombotic neutrophil extracellular traps (NETs) mediated by RAGE, exposing ad
206 iew, we examine the evidence that neutrophil extracellular traps (NETs) play a critical role in innat
207 There is emerging evidence that neutrophil extracellular traps (NETs) play important roles in infla
208 crystals became enmeshed in the neutrophilic extracellular traps (NETs) produced from host cells in r
213 ded, into the bloodstream to form neutrophil extracellular traps (NETs) that confine and kill circula
215 , we analyzed the contribution of neutrophil extracellular traps (NETs) to the mediation of protectio
216 ial invasion, neutrophils release neutrophil extracellular traps (NETs) to trap and kill extracellula
217 Here we report that ANCA induces neutrophil extracellular traps (NETs) via receptor-interacting prot
218 morhonuclear granulocytes to form neutrophil extracellular traps (NETs) was determined using fluoresc
219 Moreover, increased release of neutrophil extracellular traps (NETs) was observed, which was most
220 tate-acetate-induced formation of neutrophil extracellular traps (NETs) was reduced in affected cells
224 o an ionomycin-induced release of neutrophil extracellular traps (NETs), a meshwork of decondensed ch
225 nic bacteria and an impaired ability to form extracellular traps (NETs), an important neutrophil func
227 17 recruits neutrophils, triggers neutrophil extracellular traps (NETs), and excludes cytotoxic CD8 T
228 y aimed to explore the release of neutrophil extracellular traps (NETs), associated antimicrobial pro
229 ned the relationships between CLS neutrophil extracellular traps (NETs), bacterial components as trig
230 depends on their ability to form neutrophil extracellular traps (NETs), but the underlying mechanism
231 kill large pathogens by releasing neutrophil extracellular traps (NETs), but whether they target hook
232 ve oxygen species, and release of neutrophil extracellular traps (NETs), can result in severe patholo
233 he yeast and subsequently release neutrophil extracellular traps (NETs), complexes of DNA, histones,
237 tinal lumen, which appeared to be neutrophil extracellular traps (NETs), suggesting that V. cholerae
238 lacking ACT induces formation of neutrophil extracellular traps (NETs), whereas wild-type B. pertuss
240 , and granule proteins to produce neutrophil extracellular traps (NETs), which can trap microbes.
241 erminants of NTHI survival within neutrophil extracellular traps (NETs), which we have shown to be an
242 ly, LukGH promoted the release of neutrophil extracellular traps (NETs), which, in turn, ensnared but
243 f neutrophils-the ability to form neutrophil extracellular traps (NETs)-may contribute to organ damag
272 ement interacts with the platelet/neutrophil extracellular traps (NETs)/thrombin axis, using COVID-19
273 uclear leukocytes to release DNA [neutrophil extracellular traps (NETs)], thereby immobilizing microb
275 (-/-)) (enzymes that formation of neutrophil extracellular traps [NETs]), and mice with LSEC-specific
276 ) is released into the blood from neutrophil extracellular traps(NETs) in response to severe infectio
277 tion of granular constituents and neutrophil extracellular traps, neutrophils target microbes and pre
278 ation and membrane pore formation, and (iii) extracellular trapping of FGF2 mediated by heparan sulfa
279 -dose LPS-induced neutrophils and neutrophil extracellular traps potentiated the uptake of house dust
282 tion, reactive oxygen species and neutrophil extracellular trap production, and endolysosomal signali
285 ur work documents and provides details about extracellular trap release in human neutrophils activate
287 mination of linker histones links neutrophil extracellular trap release with autoantibodies in system
288 anulocyte activation causes the formation of extracellular traps, releasing web-like structures of DN
290 echanisms, including formation of neutrophil extracellular traps through a recently described distinc
291 quired to induce the formation of neutrophil extracellular traps through multiple activation pathways
292 on of reactive oxygen species and neutrophil extracellular traps, two mechanisms utilized by neutroph
294 E in cancer patients by releasing neutrophil extracellular traps whereas monocytes may express TF.
295 its bactericidal activity and to neutrophil extracellular traps, whereas an FnBPB-overexpressing mut
296 ere was also a decrease in plaque neutrophil extracellular traps, which are atherogenic and increased
297 us to initiate DNA extrusion into neutrophil extracellular traps, which bind NE and cathepsin G.
299 ils displayed a greater tendency to protrude extracellular traps, which were more strongly incorporat
300 neutrophils affected formation of neutrophil extracellular traps while not influencing phagocytosis,