コーパス検索結果 (１語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 n pathogenicity was not due to resistance to neutrophil extracellular traps.
2 dependent production of highly prothrombotic neutrophil extracellular traps.
3 ctin-Fc was required to trigger formation of neutrophil extracellular traps.
4 in necrotic tissues and areas that displayed neutrophil extracellular traps.
5 ell line and can also block the formation of neutrophil extracellular traps.
6 expulsion of their nuclear contents to form neutrophil extracellular traps.
7 bacterial virulence factors and formation of neutrophil extracellular traps.
8 MRSA killing by human neutrophils and within neutrophil extracellular traps.
9 ration of reactive oxygen species (ROS), and neutrophil extracellular traps.
10 ing through phagocytosis, degranulation, and neutrophil extracellular traps.
11 s after surgery, which generated luminal DNA neutrophil extracellular traps.
12 ssociated with proteases, which are known as neutrophil extracellular traps.
13 rculating microparticles, cell-free DNA, and neutrophil extracellular traps.
14 DG concerning phagocytosis and generation of neutrophil extracellular traps.
15 the chemokine receptor CXCR4 and to release neutrophil extracellular traps.
16 in the formation of a barricade comprised of neutrophil extracellular traps.
17 ayed a marked impairment in the formation of neutrophil extracellular traps, a bactericidal mechanism
18 e in vivo was revealed with the discovery of neutrophil extracellular traps, a specialized cell death
19 se 4, an enzyme important for the release of neutrophil extracellular traps, abolished neutrophil agg
20 e to microbial killing, trigger formation of neutrophil extracellular traps and appear to partake in
21 Histones are the major protein components of neutrophil extracellular traps and are known to have cyt
23 t GAS from killing by neutrophils and within neutrophil extracellular traps and neutralizes LL-37 che
24 tion-sensitized' neutrophils, as well as the neutrophil extracellular traps and other products made b
25 elf-DNA (eg, released from dying cells or in neutrophil extracellular traps) and an increased express
26 tional substrate of PAD4, localize H1 within neutrophil extracellular traps, and detect autoantibodie
27 IT-4 decreases mtDNA release, IFN signaling, neutrophil extracellular traps, and disease severity in
28 phils to capture exogenous material, extrude neutrophil extracellular traps, and kill bacteria via ca
29 ribe the new players, such as polyphosphate, neutrophil extracellular traps, and microparticles, whic
30 lm formation, decreases bacterial killing by neutrophil extracellular traps, and modulates S. pyogene
31 peptides and reactive oxygen species, escape neutrophil extracellular traps, and promote and accelera
32 ent-mediated lysis, engulfment, formation of neutrophil extracellular traps, and release of antimicro
33 binds to genomic DNA, mitochondrial DNA, and neutrophil extracellular traps, and shuttles them in the
34 is known to interfere with the formation of neutrophil extracellular traps, appears to prolong lysis
36 of type 1 IFN by pDCs, which were induced by neutrophil extracellular traps arising from the endocyto
38 report that an increase in the deployment of neutrophil extracellular traps associated with hyperglyc
39 t in the lung, kidney, and heart, containing neutrophil extracellular traps associated with platelets
42 ever, neutrophils were less prone to undergo neutrophil extracellular traps cell death in the tissue
43 ericidal activity and enhanced production of neutrophil extracellular traps compared with wild-type n
44 nse self-DNA released from dying cells or in neutrophil extracellular traps complexed to the antimicr
48 This defense mechanism is reminiscent of the neutrophil extracellular traps (ETs) recently described
49 e related to their unique ability to release neutrophil extracellular traps even in the absence of pa
52 se of forming biofilms, where they underwent neutrophil extracellular trap formation (NETosis) in res
53 deiminase type IV), an enzyme essential for neutrophil extracellular trap formation (NETosis), is re
55 , length, myeloid cell recruitment, and more neutrophil extracellular trap formation (NETs) in WT com
56 tly induce plasmatic coagulation but induced neutrophil extracellular trap formation and DNA release
57 ls, stimulated cytokine release, and induced neutrophil extracellular trap formation and myeloperoxid
58 ndependent mechanism that is associated with neutrophil extracellular trap formation and selective au
60 s prevented in transgenic mice with impaired neutrophil extracellular trap formation and/or neutrophi
61 which also exhibited an elevated capacity in neutrophil extracellular trap formation at baseline and
62 cient cells showed a significant increase in neutrophil extracellular trap formation but were unable
63 ells harboring bacteria and an impairment of neutrophil extracellular trap formation in vivo during K
64 ession by myeloid cells, but did not require neutrophil extracellular trap formation involving peptid
65 egulated protein 78, and reduced spontaneous neutrophil extracellular trap formation of bone marrow-d
66 enhanced alphaMbeta2 integrin activation and neutrophil extracellular trap formation under inflammato
67 cellular killing and were fully competent in neutrophil extracellular trap formation, a recently iden
68 ines, more severe pulmonary edema, increased neutrophil extracellular trap formation, and elevated co
69 asing histone-induced neutrophil congestion, neutrophil extracellular trap formation, and thrombosis
70 ectin shedding, oxidative burst, chemotaxis, neutrophil extracellular trap formation, bacterial killi
71 acterized by increased leukocyte engagement, neutrophil extracellular trap formation, fibrin, and loc
72 ciated vasculitis and controls, and assessed neutrophil extracellular trap formation, reactive oxygen
73 ro, AZM198 led to a significant reduction in neutrophil extracellular trap formation, reactive oxygen
80 tients with severe disease display excessive neutrophil extracellular traps formation, neutrophil-inf
81 ence of innate cell activation that included neutrophil extracellular trap generation and elevated su
82 trophil response, and we present evidence of neutrophil extracellular trap generation during experime
83 il depletion or inhibition of the release of neutrophil extracellular traps had little effects, but p
84 ysregulation in RA, their ability to extrude neutrophil extracellular traps has recently been implica
87 damage to fungal filaments, suggesting that neutrophil extracellular traps help to protect the epith
88 bind DNA strongly and localize to nuclei and neutrophil extracellular traps in a DNA-dependent manner
89 us on current findings of the involvement of neutrophil extracellular traps in atherogenesis and athe
90 creased expression of Cramp and formation of neutrophil extracellular traps in atherosclerotic arteri
92 +/- 122.4 ng/mL; p </= 0.05) and identified neutrophil extracellular traps in kidney and liver tissu
93 as a cancer biomarker and (v) implication of neutrophil extracellular traps in tumorigenesis are disc
95 ocarditis rat model, we identified layers of neutrophil extracellular traps interconnecting and entra
96 ial responses to its advantage by converting neutrophil extracellular traps into a bacterial weapon a
97 rmation (NETosis), is released together with neutrophil extracellular traps into the extracellular mi
98 ia is known to counteract histone as well as neutrophil extracellular trap-mediated cytotoxicity agai
99 eparan sulfate proteoglycan(s) is present in neutrophil extracellular traps, modulates histone affini
100 her this causes extracellular DNA (eDNA) and neutrophil extracellular trap (NET) accumulation in the
101 PMNs mount a fulminant and self-propagating neutrophil extracellular trap (NET) and cytokine respons
106 s binding to immobilized neutrophils induced neutrophil extracellular trap (NET) formation in respons
107 ed a novel role for heme in the induction of neutrophil extracellular trap (NET) formation in SCD.
109 in extensive immune infiltration with robust neutrophil extracellular trap (NET) formation in the ske
110 C3HeB/FeJ mice) result in type I IFN-induced neutrophil extracellular trap (NET) formation that promo
111 1) expression of IL-4 receptor subunits, (2) neutrophil extracellular trap (NET) formation, (3) migra
112 agocytic reactive oxygen species production, neutrophil extracellular trap (NET) formation, and neutr
113 detail which neutrophil functions, including neutrophil extracellular trap (NET) formation, are invol
121 phagocytosis, oxidative burst capacity, and neutrophil extracellular trap (NET) generation (NETosis)
123 ophil recruitment, platelet aggregation, and neutrophil extracellular trap (NET) release in the liver
124 release of granule proteins with subsequent neutrophil extracellular trap (NET) release independent
128 bacterial and host components that included neutrophil extracellular trap (NET) structures and that
129 ce factors and allows the bacterium to avoid neutrophil extracellular trap (NET)-mediated killing.
133 latelet-neutrophil complexes, a signature of neutrophil extracellular traps (NET), in the kidneys of
136 olving apoptosis and cell death by releasing neutrophil extracellular traps (NETs) (NETosis), which w
137 h of infection, neutrophils start to release neutrophil extracellular traps (NETs) against Acinetobac
139 Eros also contributes to the formation of neutrophil extracellular traps (NETS) and impacts on the
140 ed that Scl-1 mediates bacterial survival in neutrophil extracellular traps (NETs) and protects GAS f
141 in the activation of leukocytes, release of neutrophil extracellular traps (NETs) and severe inflamm
143 ecruitment, activation, and the formation of neutrophil extracellular traps (NETs) and to elucidate t
162 reactive oxygen species (ROS) and release of neutrophil extracellular traps (NETs) by activated neutr
166 ils play a crucial role in sepsis, releasing neutrophil extracellular traps (NETs) composed of DNA co
179 atory von Willebrand factor) and presence of neutrophil extracellular traps (NETs) have been implicat
183 w that these particles induce the release of neutrophil extracellular traps (NETs) in a size-dependen
185 be explained by the mitigation of increased neutrophil extracellular traps (NETs) in diabetic wounds
186 eration of reactive oxygen species (ROS) and neutrophil extracellular traps (NETs) in mouse and human
187 l activation and release of IL-1beta-bearing neutrophil extracellular traps (NETs) in patients with F
188 sensed microbe size and selectively released neutrophil extracellular traps (NETs) in response to lar
189 rom this patient were incapable of producing neutrophil extracellular traps (NETs) in response to ROS
190 t human neutrophils release large amounts of neutrophil extracellular traps (NETs) in the presence of
191 e most recent findings regarding the role of neutrophil extracellular traps (NETs) in thrombosis.
193 activated platelets induce the formation of neutrophil extracellular traps (NETs) in transfusion-rel
195 oxygen species in the phagosome and release neutrophil extracellular traps (NETs) into their surroun
197 cardiomyocytes and the possible formation of neutrophil extracellular traps (NETs) may result in chro
199 in vitro, but neutrophil products including neutrophil extracellular traps (NETs) mediate host organ
200 HMGB1 facilitates formation of prothrombotic neutrophil extracellular traps (NETs) mediated by RAGE,
202 In this review, we examine the evidence that neutrophil extracellular traps (NETs) play a critical ro
208 , DNA included, into the bloodstream to form neutrophil extracellular traps (NETs) that confine and k
210 this study, we analyzed the contribution of neutrophil extracellular traps (NETs) to the mediation o
211 e to microbial invasion, neutrophils release neutrophil extracellular traps (NETs) to trap and kill e
213 olated polymorhonuclear granulocytes to form neutrophil extracellular traps (NETs) was determined usi
215 orbol-myristate-acetate-induced formation of neutrophil extracellular traps (NETs) was reduced in aff
219 sceptible to an ionomycin-induced release of neutrophil extracellular traps (NETs), a meshwork of dec
221 red that IL17 recruits neutrophils, triggers neutrophil extracellular traps (NETs), and excludes cyto
222 This study aimed to explore the release of neutrophil extracellular traps (NETs), associated antimi
223 We examined the relationships between CLS neutrophil extracellular traps (NETs), bacterial compone
224 rategies to eliminate pathogens they release neutrophil extracellular traps (NETs), being chromatin f
225 hils partly depends on their ability to form neutrophil extracellular traps (NETs), but the underlyin
226 cytes that kill large pathogens by releasing neutrophil extracellular traps (NETs), but whether they
227 n of reactive oxygen species, and release of neutrophil extracellular traps (NETs), can result in sev
228 agocytose the yeast and subsequently release neutrophil extracellular traps (NETs), complexes of DNA,
230 named NETosis, characterized by formation of neutrophil extracellular traps (NETs), decondensed chrom
232 leased into blood, through the generation of neutrophil extracellular traps (NETs), is procoagulant a
233 DNA release associated with the formation of neutrophil extracellular traps (NETs), known as NETosis.
234 n the intestinal lumen, which appeared to be neutrophil extracellular traps (NETs), suggesting that V
235 . pertussis lacking ACT induces formation of neutrophil extracellular traps (NETs), whereas wild-type
237 have reported that human neutrophils release neutrophil extracellular traps (NETs), which are protein
238 A, histones, and granule proteins to produce neutrophil extracellular traps (NETs), which can trap mi
239 nflammatory stimuli and pathogens, they form neutrophil extracellular traps (NETs), which capture and
240 portant determinants of NTHI survival within neutrophil extracellular traps (NETs), which we have sho
241 Unexpectedly, LukGH promoted the release of neutrophil extracellular traps (NETs), which, in turn, e
242 function of neutrophils-the ability to form neutrophil extracellular traps (NETs)-may contribute to
275 d how complement interacts with the platelet/neutrophil extracellular traps (NETs)/thrombin axis, usi
276 polymorphonuclear leukocytes to release DNA [neutrophil extracellular traps (NETs)], thereby immobili
278 LDGs have heightened capacity to synthesize neutrophils extracellular traps (NETs), which display in
279 pe IV (Pad4(-/-)) (enzymes that formation of neutrophil extracellular traps [NETs]), and mice with LS
280 ne H3(CitH3) is released into the blood from neutrophil extracellular traps(NETs) in response to seve
281 nts, activation of granular constituents and neutrophil extracellular traps, neutrophils target micro
285 f degranulation, reactive oxygen species and neutrophil extracellular trap production, and endolysoso
288 th altered neutrophil expression of ISGs and neutrophil extracellular trap release is not known.
290 ract neutrophils, triggering the ejection of neutrophil extracellular traps that contain nuclear prot
291 y various mechanisms, including formation of neutrophil extracellular traps through a recently descri
292 eria are required to induce the formation of neutrophil extracellular traps through multiple activati
293 he production of reactive oxygen species and neutrophil extracellular traps, two mechanisms utilized
294 a harvested from morning saliva had released neutrophil extracellular traps (undergone NETosis) in vi
295 increase VTE in cancer patients by releasing neutrophil extracellular traps whereas monocytes may exp
296 ceptible to its bactericidal activity and to neutrophil extracellular traps, whereas an FnBPB-overexp
298 o the nucleus to initiate DNA extrusion into neutrophil extracellular traps, which bind NE and cathep
300 in mutant neutrophils affected formation of neutrophil extracellular traps while not influencing pha