ライフサイエンスコーパス: neutrophil

1 mass from mature biofilms in the presence of neutrophils.

2 atients, notably those with greater than 61% neutrophils.

3 edge, the role of PIKfyve in human and mouse neutrophils.

4 ancing parasite clearance by macrophages and neutrophils.

5 abling them to recruit APRIL-producing blood neutrophils.

6 porters, SLC and ABC, in resting human blood neutrophils.

7 g the adherence, migration and activation of neutrophils.

8 gnificantly increased phagocytic capacity of neutrophils.

9 uction of oxidized compounds by infiltrating neutrophils.

10 s in the nerve, and elevated phagocytosis by neutrophils.

11 xtracellular traps (NETs) in mouse and human neutrophils.

12 ntracellular carriers for drug delivery into neutrophils.

13 Pases was markedly increased in miR-142(-/-) neutrophils.

14 escued the NET formation defect in Mincle-/- neutrophils.

15 et interactions in AMI patients by targeting neutrophils.

16 s associated with increased killing by human neutrophils.

17 g, suggesting a form of quorum sensing among neutrophils.

18 rs of immune suppressive CD16BRIGHT CD62LDIM neutrophils (82.07 x 106/l +/- 18.94 control versus 1,09

19 ection of diphtheria toxin induces selective neutrophil ablation.

20 Neutrophils accumulate in SLO over the course of lupus p

21 oted downstream endothelial cell activation, neutrophil accumulation, endothelial cell death and desq

22 Type I IFN-mediated neutrophil activation and NET formation may contribute t

23 Genes associated with neutrophil activation, ROS production, intracellular ant

24 or Stim2 to investigate the role of STIM2 in neutrophil activation.

25 d calcium entry (SOCE) are known to regulate neutrophil activation; however, the precise mechanism of

26 ession analysis following nuclear RNA-seq of neutrophil active transcriptomes reveals a significant u

27 neutrophilic source and provides evidence of neutrophil activity on the ocular surface of oGVHD patie

28 nterfering RNA in endothelial cells enhanced neutrophil adhesion to endothelial cells but inhibited n

29 IFN-alpha treatment also led to enhanced neutrophil adhesion.

30 d intracellular ROS were measured in healthy neutrophils after treatment with purified albumin from t

31 ms, an enrichment of ILC2s, eosinophils, and neutrophils, along with increased production of IL-5, pr

32 In this article, we show that human neutrophils altered their expression of IL-20R chains up

33 Clusters 2, 3, and 4 were associated with neutrophil and lymphocyte frequencies and neutrophil/lym

34 vitro models of lipopolysaccharide-mediated neutrophil and macrophage activation.

35 inhibitory factor, and chemokines mediating neutrophil and monocyte infiltration.

36 Myeloperoxidase (MPO) is synthesized by neutrophil and monocyte precursor cells and contributes

37 Neutrophil and NK cell infiltration and capillary thromb

38 ANCA activates neutrophils and activated neutrophils damage the endothe

39 ges and T cells, with less contribution from neutrophils and B cells.

40 S6 was mediated by BLT-1 in healthy subject neutrophils and by ERV-1 in diabetes.

41 oduction of IL-1beta, activate platelets and neutrophils and elevate blood pressure in mice.

42 immune response is dominated by infiltrating neutrophils and elicits a mixed TH17/TH1 response.

43 d cancer (CAC) and inhibits the expansion of neutrophils and granulocytic myeloid-derived suppressor

44 Older thrombi contained significantly more neutrophils and H3Cit compared to fresh thrombi.

45 Neutrophils and IL-17A have been linked mechanistically

46 tran sodium sulfate, colonic infiltration of neutrophils and inflammatory cytokine production are imp

47 he Asp358Ala variant in sIL-6R shedding from neutrophils and its pro-inflammatory effects in the lung

48 e prominently expressed in wound-infiltrated neutrophils and macrophages and play central roles in wo

49 AA fragments failed to directly chemoattract neutrophils and monocytes, to induce chemokines and to s

50 nnate immune cells into the tumors including neutrophils and NK cells and suppressed tumor progressio

51 tein kinase phosphatase-1 were determined in neutrophils and peripheral blood mononuclear cells.

52 rdial infarction, with increased circulating neutrophils and platelets, consistent with increased car

53 RA was associated with increased numbers of neutrophils and proneutrophilic biomolecules in the airw

54 immunoglobulin G (IgG) and polymorphonuclear neutrophils and show the importance of an antibody/effec

55 We sought to investigate the role of neutrophils and the IL-17A pathway in mediating pediatri

56 RvE1 binds to leukotriene B4 (BLT-1) on neutrophils and to ERV-1/ChemR23 on monocyte/macrophages

57 otoxicity, viral response, B cell, platelet, neutrophil, and mast cell/basophil activity.

58 criptional response to PKA activation in the neutrophil, and that they positively regulate neutrophil

59 eased vascular permeability, fewer pulmonary neutrophils, and a reduction in levels of neutrophil che

60 ck, improving phagocytic killing activity of neutrophils, and preventing bacterial adherence to lung

61 ce, promoted phagocytosis by macrophages and neutrophils, and protected mice from MRSA infection in t

62 m strains stimulated significant increase in neutrophil apoptosis compared with control (P <0.001) an

63 ise, the ability of ROL or Bt2cAMP to induce neutrophil apoptosis was impaired in AnxA-knock-out mice

64 ever, it is now increasingly recognized that neutrophils are a heterogeneous population, and a more p

65 Neutrophils are a major source of OSM-producing cells in

66 Neutrophils are among the immune cells that can drive th

67 se with a high percentage of olfactomedin-4+ neutrophils are at higher risk for greater organ failure

68 ic aggregation nor NETosis occurs when human neutrophils are exposed either to immobilized fungal bet

69 Neutrophils are recognised to play a pivotal role at the

70 with lung squamous cell carcinoma, and that neutrophils are the most prevalent immune cell type.

71 Wiskott-Aldrich syndrome protein-deficient neutrophils are unable to polymerize actin and exhibit a

72 onse genes at early times post-exposure, and neutrophil-associated genes at later time points.

73 TH2-driven eosinophilic inflammation and neutrophil-associated inflammasome activation might repr

74 f B cell self-tolerance in vivo, we depleted neutrophils at different stages of disease.

75 sites had massive numbers of and few intact neutrophils at the edge and center of the infection site

76 functions for STIM1 and STIM2 in modulating neutrophil bactericidal and cytokine responses.

77 ecific skin innate responsiveness to Hla and neutrophil bactericidal capacity play important roles in

78 the numbers of activated infiltrating murine neutrophils but not neutrophil cellularity.

79 as apparent also, though less abundantly, in neutrophils, but not in lymphocytes.

80 ired for Mtb growth after uptake of infected neutrophils by human macrophages.

81 cAMP blocks the oxidative burst capacity of neutrophils by two converging mechanisms.

82 by macrophages, but if apoptosis is delayed, neutrophils can cause extensive tissue damage and chroni

83 r well-established antimicrobial properties, neutrophils can contribute to optimal host protection by

84 edge, these data are the first evidence that neutrophils can undergo subtype differentiation in vitro

85 d adherence, circulating neutrophil numbers, neutrophil CD11b expression, and myeloperoxidase activit

86 ated infiltrating murine neutrophils but not neutrophil cellularity.

87 ry neutrophils, and a reduction in levels of neutrophil chemoattractant CXCL1 in their lungs compared

88 from the Cancer Genome Atlas showed that the neutrophil chemokine CXCL1 gene was highly upregulated i

89 c nerves demonstrate prolonged expression of neutrophil chemokines, a concomitant extended increase i

90 disorders, GPP, PPP, and AGEP, converged on neutrophil chemotaxis and diapedesis and cytokines known

91 ntribute to chronic inflammation by inducing neutrophil chemotaxis, and the reduction of these microv

92 duced the ability of keratinocytes to induce neutrophil chemotaxis.

93 mes revealed declining radii of gyration for neutrophil chromosomes.

94 ll dynamics and promoted neovascularization, neutrophil clearance, cardiomyocyte proliferation and sc

95 ge recruitment in medaka, along with delayed neutrophil clearance.

96 oll-like receptors were overexpressed in SAH neutrophils compared to healthy neutrophils (P < 0.05).

97 f H3Cit with extracellular DNA released from neutrophils confirmed the specific presence of NETs.

98 WASP depletion from human neutrophils confirms that both proteins are involved in

99 Neutrophils could increase VTE in cancer patients by rel

100 mmon grade 3-4 adverse events were decreased neutrophil count (210 [37%] in the cetuximab group vs 15

101 vacizumab group), and infections with normal neutrophil count (42 events vs 53).

102 ere decreased lymphocyte (n=3) and decreased neutrophil count (n=2); and grade 4 anaemia was reported

103 For two traits, lipoprotein(a) levels and neutrophil count, aggregate tests of low-frequency and r

104 s in CD4 cell count, but not by increases in neutrophil count.

105 ts, mortality was associated with higher CSF neutrophil counts (hazard ratio [HR], 1.10 per 10% incre

106 risk factors and acute conditions affecting neutrophil counts (such as infections and cancer).

107 Adjusted HRs comparing neutrophil counts 6 to 7 versus 2 to 3 x 10(9)/l (both w

108 In Hbb(th3/+) mice, the expression of neutrophil CXCR2, CD11b, and reduced NAD phosphate oxida

109 However, neutrophil cytokine production required STIM2, but not S

110 ve stress response to hyperglycemia perturbs neutrophil cytoskeletal stability leading to MP producti

111 ANCA activates neutrophils and activated neutrophils damage the endothelium, leading to vascular

112 Neutrophil density in the bronchial mucosa was similar a

113 e data indicate that in this model of acute, neutrophil-dependent glomerulonephritis, NETs are genera

114 important inhibitory role in local IL-1- and neutrophil-dependent tissue inflammation as shown in the

115 However, neutrophil depletion abrogated protection from death in

116 ng experimental liver metastases phenocopied neutrophil depletion by reducing liver metastatic colony

117 Systemic neutrophil depletion was found to render wild-type mice

118 we found that in response to hyperglycemia, neutrophil-derived S100 calcium-binding proteins A8/A9 (

119 rculating platelet-leukocyte aggregates, and neutrophils displayed a greater tendency to protrude ext

120 phagocytic clearance compelling alternative neutrophil effector mechanisms to destroy these physical

121 observed in NPs, showed colocalization with neutrophil elastase (n = 10), and did not colocalize wit

122 inhibitor) expression and downregulation of neutrophil elastase (NE) expression induced by obstructi

123 To investigate the levels of neutrophil elastase (NE), matrix metalloproteinases (MMP

124 RATIONALE: Sputum neutrophil elastase and serum desmosine, which is a link

125 phil extracellular trap (NET) formation, and neutrophil elastase translocation.

126 se model of peritonitis, we demonstrate that neutrophils elicited in the presence of C-type lectin re

127 hese data were translated by assessing human neutrophil-endothelial interactions under flow: PD1n-3 D

128 three distinct datasets: in vivo response of neutrophils evoked by systemic endotoxin challenge, the

129 To assess whether neutrophils exert predominantly protective or deleteriou

130 However, CD177(pos) neutrophils exhibit no clear migratory advantage in vivo

131 Activated TTP-deficient neutrophils exhibited decreased apoptosis and enhanced a

132 um of asthma severity, but the percentage of neutrophils expressing CEACAM6 was significantly increas

133 agocytic reactive oxygen species production, neutrophil extracellular trap (NET) formation, and neutr

134 ence of innate cell activation that included neutrophil extracellular trap generation and elevated su

135 eration of reactive oxygen species (ROS) and neutrophil extracellular traps (NETs) in mouse and human

136 elease their nuclear material in the form of neutrophil extracellular traps (NETs).

137 us on current findings of the involvement of neutrophil extracellular traps in atherogenesis and athe

138 y various mechanisms, including formation of neutrophil extracellular traps through a recently descri

139 increase VTE in cancer patients by releasing neutrophil extracellular traps whereas monocytes may exp

140 e in vivo was revealed with the discovery of neutrophil extracellular traps, a specialized cell death

141 lm formation, decreases bacterial killing by neutrophil extracellular traps, and modulates S. pyogene

142 F showed the highest and fastest recovery of neutrophils, followed by GCSF-Fc and GCSF.

143 Priming neutrophils for an enhanced respiratory burst together w

144 However, circulating neutrophils form unstable aggregates and are unexpectedl

145 Mature neutrophils from Hbb(th3/+) mice displayed a significant

146 A similar phenomenon was also observed in neutrophils from healthy controls exposed to patient pla

147 Additionally, neutrophils from hPR3Tg displayed enhanced survival duri

148 Neutrophil function was reduced for 28 days postburn inj

149 tive regulation of both fibrin formation and neutrophil function.

150 TIPSS insertion renders this neutrophil functional defect systemic, associated with a

151 to define the effects of these mediators on neutrophil functions and the underlying cellular mechani

152 RATIONALE: Dysregulated neutrophil functions with age and sepsis are described.

153 label-free electrochemical immunosensor for neutrophil gelatinase-associated lipocalin (NGAL) detect

154 group (P = 0.0004), and was noninferior for neutrophil gelatinase-associated lipocalin [14.7 mug/L (

155 pe plasminogen activator receptor, suPAR and neutrophil gelatinase-associated lipocalin, NGAL.

156 Compared to biofilm, neutrophils generate higher levels of reactive oxygen sp

157 In neutrophils, genes with hypervariable expression are fou

158 Tumor-infiltrating neutrophils have been implicated in malignant developmen

159 Neutrophil(high) patients also had better symptom contro

160 ced significant chemotaxis of isolated mouse neutrophils in a Tie2- and CD18-dependent manner.

161 suggest a predominantly protumoral role for neutrophils in cancer development.

162 To study the role of neutrophils in LPS-induced endotoxemia, we developed a n

163 Olfactomedin-4 identifies a subpopulation of neutrophils in patients with septic shock, and those wit

164 tial beneficial rather than adverse role for neutrophils in pediatric severe asthma pathophysiology.

165 uded the activation state of eosinophils and neutrophils in peripheral blood to phenotype and monitor

166 emodeling, changes associated with decreased neutrophils in the heart.

167 ion of inflammatory monocyte macrophages and neutrophils in the lungs of male mice, and depletion of

168 ant extended increase in the accumulation of neutrophils in the nerve, and elevated phagocytosis by n

169 ncreased numbers of activated mast cells and neutrophils in the perivascular area of atherosclerotic

170 pathogen for periodontitis, revealed reduced neutrophils in TLR9(-/-) mice on day 1 postinfection com

171 SM production (P < .001) in peripheral blood neutrophils in vitro.

172 s, and fibroblasts, but IL-1R2 deficiency on neutrophils increased the IL-1-induced response of fibro

173 ae modulates mRNA and miR expression by lung neutrophils, increasing their ability to respond and fac

174 uld be explored as a potential treatment for neutrophil-induced inflammation.

175 eukocytes composed mainly of macrophages and neutrophils infiltrate infected DRGs and account for the

176 ed to the cell of origin, as APRIL-producing neutrophils infiltrated CXCL-8(+) DLBCL from both germin

177 kin inflammation characterized by T cell and neutrophil infiltration and a Th17-biased cytokine respo

178 Three days after ligation, neutrophil infiltration into ischemic limbs of AMPKalpha

179 tic fibrosis, are characterized by excessive neutrophil infiltration into the airspace.

180 e using photosensitization rapidly activates neutrophil infiltration that mediates delivery of nanoth

181 This promoted neutrophil infiltration, tumor cell (TC) adhesion to the

182 s were investigated: cell death (apoptosis), neutrophil influx and cytokine/chemokine expression.

183 t changes in endometrial apoptosis preceding neutrophil influx and cytokine/chemokine induction durin

184 flammatory condition in which ANCA-activated neutrophils interact with the endothelium, resulting in

185 Efficient removal of infected and dying neutrophils is required to protect the surrounding tissu

186 Impaired integrin activation on neutrophils is the hallmark of leukocyte adhesion defici

187 n, as well as in other cellular functions in neutrophils, is poorly understood.

188 CDK6, in neutrophils, is required for clearance of the fungal pat

189 ent also attenuated the respiratory burst of neutrophils isolated from chronic plus binge alcohol fed

190 Neutrophils isolated from mice and human subjects were t

191 Neutrophils isolated from patients spontaneously produce

192 4), and blood neutrophilia (HR, 1.06 per 109 neutrophils/L increase; 95% CI, 1.03-1.10).

193 -1 antagonism were abolished by reducing the neutrophil load with in vivo administration of an anti-L

194 anti-MPO GN suggest that, after ANCA-induced neutrophil localization, deposited MPO within glomeruli

195 Neutrophil loss-of-function limited these findings.

196 Here, we have analysed neutrophil-lymphatic vessel interactions in real time an

197 s that quantifies the population dynamics of neutrophil, lymphocyte, and monocyte characteristics.

198 or serum sodium, and pretransplant recipient neutrophil-lymphocyte ratio.

199 th neutrophil and lymphocyte frequencies and neutrophil/lymphocyte ratio after the allergen challenge

200 to IL-1beta in the tested cell types, i.e., neutrophils, macrophages, and fibroblasts, but IL-1R2 de

201 dative phosphorylation, and is essential for neutrophil maturation.

202 N status resulted in decreased resistance to neutrophil-mediated killing, which resulted in selection

203 tem, we found that CD177(pos) and CD177(neg) neutrophils migrated comparably.

204 egulatory mediator involved in modulation of neutrophil migration throughout the course of neutrophil

205 The antimigratory effect of Sema3E on human neutrophil migration was associated with suppression of

206 To assess neutrophil migratory accuracy with age during respirator

207 rotect the surrounding tissue from bioactive neutrophil molecules and subsequent pathological sequela

208 Neutrophil myeloperoxidase (MPO) catalyzes the H2O2-depe

209 deconvolution analysis identifies changes in neutrophil, naive CD4(+) T cell, and macrophage populati

210 Neutrophil necrosis was required for Mtb growth after up

211 Defects in neutrophil number and survival are common to both hemato

212 Although neutrophil numbers at baseline and 8 hours were greater

213 rease in the affected kidneys, whereas renal neutrophil numbers were not affected.

214 leukocyte rolling and adherence, circulating neutrophil numbers, neutrophil CD11b expression, and mye

215 In neutrophils of sepsis patients, mitogen activated protei

216 orter 2 inhibitor (dapagliflozin), depleting neutrophils or Kupffer cells, or inhibiting S100A8/A9 bi

217 spectively, on day 1 and were full of intact neutrophils or necrotic cells on day 2.

218 tracellular labile iron that is required for neutrophil oxidative responses.

219 essed in SAH neutrophils compared to healthy neutrophils (P < 0.05).

220 ly increased expression of NF-kappaB mRNA in neutrophils (P <0.05).

221 sthma, suggesting the presence of an altered neutrophil phenotype.

222 The concept of neutrophil plasticity is new and, to our knowledge, thes

223 Metoprolol inhibits neutrophil-platelet interactions in AMI patients by targ

224 Neutrophils play a crucial role in host defense.

225 Neutrophils play a key role in host defenses and have re

226 ously, we demonstrated the requirement for a neutrophil (PMN) subset expressing CD49d to drive develo

227 ffected the recruitment of polymorphonuclear neutrophils (PMN) to bacterial and fungal pathogens as w

228 ulmonary epithelium and on polymorphonuclear neutrophil (PMNs) after transepithelial migration into t

229 Trafficking of polymorphonuclear neutrophils (PMNs) during inflammation critically depend

230 fatty acids from intracellular stores within neutrophil precursor cells.

231 scued differentiation in autophagy-deficient neutrophil precursors.

232 We previously found that neutrophils produce and release Eosinophil Cationic Prot

233 Neutrophils pulsed with the cognate antigens cytomegalov

234 al IL-17F(+) cells correlated with bronchial neutrophils (r = 0.54), exacerbation rate (r = 0.41), an

235 (r=0.54; P<0.005) and inversely with sputum neutrophils (r=-0.46: P<0.05), but not with FEV1 (% pred

236 hat immediately after bacteria-cell contact, neutrophils rapidly and continuously engulf and kill bac

237 The stool microbiota around the time of neutrophil recovery post-HCT is predictive of subsequent

238 r after transplantation of BM and PB (28-day neutrophil recovery, 88% v 93%, P = .07; 100-day platele

239 t that CCRL2-deficient mice have a defect in neutrophil recruitment and are protected in 2 models of

240 ition of this chemotaxis abolished increased neutrophil recruitment and tumor metastasis.

241 gnaling axis identified HIF-2alpha-dependent neutrophil recruitment as an essential mechanism to incr

242 ly, suppressing IL-1beta expression to limit neutrophil recruitment as each phagocyte eliminated nume

243 vidual animals revealed that the blocking of neutrophil recruitment leads to rapid mortality in this

244 rate that HIF-2alpha is a novel regulator of neutrophil recruitment to colon tumors and that it is es

245 CXCR2 is an essential regulator of neutrophil recruitment to inflamed and damaged sites and

246 2alpha-overexpressing mice demonstrated that neutrophil recruitment was a direct response to increase

247 factor (TNF) and interleukin-6 (IL-6), more neutrophil recruitment, and a lower bacterial load in lu

248 associated with reduced lung injury, reduced neutrophil recruitment, and lower cytokine levels.

249 ed to induce robust vaginal immunopathology (neutrophil recruitment, interleukin-1beta [IL-1beta] sec

250 duced lung injury in a manner independent of neutrophil recruitment, which we postulate instead arise

251 NETosis is a physiologic process in which neutrophils release their nuclear material in the form o

252 Following 72 h ambient storage, neutrophils remained fully functional to migrate towards

253 identical in WT and Ccr2(-/-) mice, and that neutrophils replace CCR2(+) macrophages as the primary p

254 Thus, neutrophils represent a promising target to manage infla

255 Upregulation of HLA-DR on neutrophils required the presence of the antigen-specifi

256 l-like receptor 2 and CD11b on monocytes and neutrophils, respectively, were observed.

257 eater lung damage and an IL-1alpha-dependent neutrophil response.

258 ifying transcriptional and non-translational neutrophil responses, which might permit a controlled de

259 ium sensor required for classical short-term neutrophil responses.

260 and diapedesis and cytokines known to drive neutrophil-rich inflammatory processes, including IL-1 a

261 A chronic, neutrophil-rich inflammatory response characterizes this

262 and colleagues (pp. 141-153) investigate the neutrophil's genome organization and the mechanisms that

263 howed that chemokine-mediated recruitment of neutrophils secreting the tumor-promoting factor APRIL m

264 nocyte migration and with CXCL8 to stimulate neutrophil shape change and chemotaxis.

265 The expression levels of the immature-like neutrophil signature increased linearly with pregnancy,

266 analyzed in Mincle-sufficient and -deficient neutrophils stimulated in vitro with various stimuli and

267 in-4 might serve as a marker of a pathogenic neutrophil subset in patients with septic shock.

268 r these cell types represent truly different neutrophil subsets or reflect changes induced by lipopol

269 eutrophil, and that they positively regulate neutrophil survival and homeostasis.

270 Neutrophil survival in ischemic tissue is required to at

271 VLA5 and the upregulation of VLA3 to support neutrophil swarming and aggregation.

272 ether cPLA2alpha is directly responsible for neutrophil synthesis of LTB4 in the context of Pseudomon

273 Neutrophils, the front line defenders against infection,

274 nfection sites had massive numbers of intact neutrophils throughout the whole infection site.

275 teomes of banded, mature, and hypersegmented neutrophils to determine whether these cell types repres

276 t a time when the prevailing view considered neutrophils to function as nonspecific effector cells th

277 prehensive complication index (CCI), and the neutrophil-to-lymphocyte ratio (NLR) was used as an indi

278 iltration rates, higher leukocyte counts and neutrophil-to-lymphocyte ratios.

279 tivation and increased T-cell, monocyte, and neutrophil trafficking to the brain at day 8 post infect

280 he context of Pseudomonas aeruginosa-induced neutrophil transepithelial migration has not been explor

281 and three-dimensional real-time dynamics of neutrophil transepithelial migration, were applied.

282 adhesion to endothelial cells but inhibited neutrophil transmigration.

283 Such activation of neutrophils under conditions mimicking infection with S.

284 ontrols the antifungal effector functions of neutrophils under conditions that preclude phagocytosis.

285 During inflammation resolution, neutrophils undergo apoptosis before they are removed by

286 Neutrophils undergoing NETosis induced by various physio

287 s study, we deliver therapeutic compounds to neutrophils using biocompatible, nanometer-sized synthet

288 IVIG can alter the viability of human neutrophils via agonistic antibodies to Fas and Siglec-9

289 article, we report that rhAPC binds to human neutrophils via integrin VLA-3 (CD49c/CD29) with a highe

290 promotes the tissue-protecting functions of neutrophils via, at least partly, the induction of lacto

291 lectively depleted in myeloid cells, such as neutrophils, we show that FlnA negatively regulates beta

292 ine and 8 hours were greater in females, the neutrophils were less activated.

293 partments with emergence of functional mIDH2 neutrophils were observed.

294 Neutrophils were recognized as key contributors in early

295 These neutrophils were responsible for the pro-metastatic effe

296 In this study, human neutrophils were stimulated to produce NETs in platelet-

297 t subset of tumor-infiltrating SiglecF(high) neutrophils, which exhibit cancer-promoting properties.

298 dren with STRA had increased intraepithelial neutrophils, which positively correlated with FEV1 %pred

299 Similarly, neutrophils with a genetic defect in NADPH oxidase fail

300 experimentally by incubating healthy control neutrophils with soluble sputum from patients with COPD.