ライフサイエンスコーパス: PMN

1 PMN interaction with ECs induced the entry of Ca(2+) in

2 PMN migration to sites of infection/inflammation require

3 PMN TEM is associated with epithelial injury; however, m

4 PMN were shown to generate C1q and C3a; exposure of hNSC

5 PMN-conditioned NK cells displayed enhanced cytotoxicity

6 PMN-MP/MPO-dependent inhibition of IEC wound healing was

7 PMN-MPs secreted by activated PMNs during TEM displayed

8 PMNs isolated from gp91phox(-/-) mice significantly redu

9 PMNs of CP patients may be primed for low antioxidant re

10 igher quality, <10 SECs per LPF (but not >25 PMNs per LPF) was the microscopic variable most associat

11 low-power field (LPF) and 2350 (62%) had >25 PMNs per LPF, measures traditionally associated with spe

12 y on a rhombohedral Pb(Mg1/3Nb2/3)0.7Ti0.3O3(PMN-PT) ferroelectric crystal.

13 onuclear leukocytes (PMNs), with up to 10(5) PMNs in clear diluted buffer from 50 muL of airway secre

14 In humans, a PMN gene signature correlated with improved survival in

15 PMN-MPs secreted by activated PMNs during TEM displayed a high level of enzymatically

16 buted to activation of phagocytically active PMN at later time points.

17 In addition, PMN-conditioned NK cells triggered the maturation of mon

18 2578 could have additional effects affecting PMN migration.

19 ith levosimendan decreased MPO release after PMN-stimulation (8.2 +/- 1.4-fold increase at baseline v

20 In addition, Arg1 expression on CF airway PMNs correlated negatively with lung function and positi

21 ression of T cell proliferation by CF airway PMNs.

22 step, was uniformly high on CF and HC airway PMNs.

23 osis, which occurs in CF, but not HC, airway PMNs.

24 se to the TLR2/1 agonist, Pam3CSK4, although PMN from all donors were primed by the TLR2/6 agonist, F

25 sue-targeted therapies aimed at ameliorating PMN-mediated bystander-tissue damage.

26 y a critical role in VT, likely via IL-6 and PMN-mediated thrombotic mechanisms, and may be a potenti

27 a direct interaction between complement and PMN.

28 tween the effect of glibenclamide on GSH and PMN functions in response to B. pseudomallei that may co

29 but rather enhances the Il-17a induction and PMN infiltration in some mice.

30 nhibited both proteinuria and macrophage and PMN infiltration.

31 Importantly, both M-MDSCs and PMN-MDSCs showed suppression of T cell proliferation in

32 deorecorded (phase-contrast microscopy), and PMN adhesion/migration were assessed off-line.

33 inant effect on the pulmonary epithelium and PMNs.

34 ompared for different quantities of SECs and PMNs.

35 agocytosis of Escherichia coli and apoptotic PMN (efferocytosis) were enhanced with GPR18 overexpress

36 ophages was enhanced by CCL5-bound apoptotic PMN (3.6-4 fold) in a D6-dependent manner, and was essen

37 exclusively when bound to D6(+/+) apoptotic PMN.

38 tion (~40%) and enhanced uptake of apoptotic PMN (51%) by human dermal fibroblasts at concentrations

39 receptor D6/ACKR2 is expressed on apoptotic PMN and plays an important role in regulating macrophage

40 phages when acting in concert with apoptotic PMN-expressed D6.

41 ators, increasing efferocytosis of apoptotic PMNs, and stimulating local endogenous biosynthesis of S

42 e consistent with the observed aberrant ARDS PMN survival and functional phenotype that we have previ

43 The molecular mechanisms governing ARDS PMN function and longevity are incompletely understood.

44 6 showed the same directional change as ARDS PMNs.

45 showed that 1319 genes were altered in ARDS PMNs relative to healthy volunteer PMNs.

46 tabases, the gene expression profile in ARDS PMNs showed near-complete correlation to datasets derive

47 Transcripts enriched in ARDS PMNs were differentially expressed in known functional n

48 Collectively our results show that ARDS PMNs display important de-novo transcriptional activity.

49 As PMN priming by TLR4 agonists is well described, we hypot

50 ndings provide insight into tumor-associated PMNs and reveal a context-specific capacity for PMNs to

51 mechanism by which IDO induction attenuates PMN migration.

52 ydrate-mediated binding interactions between PMN Lewis glycans and endothelial glycan-binding protein

53 anding of the molecular interactions between PMNs and mucosal epithelia and the associated functional

54 Lkt from the mutant was cytotoxic to BHS PMNs in an in vitro cytotoxicity assay.

55 Blood PMNs incubated in CF airway fluid lost PD-L1 over time;

56 genomic profiling of highly pure ARDS blood PMNs in parallel with age-matched and gender-matched hea

57 wide transcriptional profiling of ARDS blood PMNs to explore underlying disease mechanisms and identi

58 In contrast, phagocytosis of C. albicans by PMN 60 min postinfection occurred almost independently o

59 tive pathogen in CGD that resists killing by PMN of CGD patients (CGD PMN) and inhibits PMN apoptosis

60 rrier for migrating PMNs, and its removal by PMN-MP-associated MMP-9 facilitates PMN trafficking acro

61 perienced lethal sepsis that was reversed by PMN expansion mediated by injection of wild-type HSPCs d

62 vosimendan treatment inhibits MPO release by PMNs in decompensated heart failure patients.

63 as rhesus M-MDSCs lacked expression of CD33, PMN-MDSCs were identified as CD33(+) low-density neutrop

64 CD49d(+) PMN frequency was significantly higher in nasal lavage f

65 e sought to determine whether human CD49d(+) PMNs are present in the nasal mucosa during acute viral

66 Similar to the mouse, human CD49d(+) PMNs isolated from nasal lavage fluid during a viral res

67 In mice CD49d(+) PMNs represented a "proatopic" neutrophil subset that ex

68 ufficient to reduce accumulation of CD49d(+) PMNs in the lungs and development of postviral atopic ai

69 enotype and functional relevance of CD49d(+) PMNs.

70 lfment of apoptotic polymorphonuclear cells (PMN) during the resolution of inflammation leads to macr

71 ear cells (MNC) and polymorphonuclear cells (PMN) to exert Ab-dependent cell-mediated cytotoxicity (A

72 BLP activated human polymorphonuclear cells (PMNs) ex vivo to adhere to denatured collagen in serum a

73 ed that neutrophil (polymorphonuclear cells [PMNs]) accumulation in culprit lesion site (CLS) thrombu

74 ion of neutrophils (polymorphonuclear cells [PMNs]) that can promote systemic spread of the infection

75 ptotic neutrophils (polymorphonuclear cells [PMNs]), production of specialized proresolving lipid med

76 lls and neutrophils (polymorponuclear cells, PMNs) succumb to M. tuberculosis within 30 days, an extr

77 d during phagocytosis by both normal and CGD PMN demonstrating responses to oxygen-independent PMN an

78 N from healthy subjects (normal PMN) and CGD PMN during incubation with G. bethesdensis and, simultan

79 bacterial resistance to both normal and CGD PMN.

80 usly, in G. bethesdensis with normal and CGD PMN.

81 genes in the presence of normal but not CGD PMN.

82 resists killing by PMN of CGD patients (CGD PMN) and inhibits PMN apoptosis through unknown mechanis

83 The goal of this study was to characterize PMN activation at the CLS.

84 CD49d and CysLTR1-coexpressing PMNs are present during symptoms of an acute viral respi

85 In the early stage of Salmonella colitis, PMNs are not required for diarrhea or for the decrease i

86 In contrast, PMN recruitment to wounds infected with an isogenic AT-d

87 Mechanisms controlling PMN extravasation have been well characterized, but the

88 The high d33 of the single-crystalline PMN-PT nanobelt results from the precise orientation con

89 METHODS AND We observed defective PMN transmigration in response to lipopolysaccharide cha

90 lammatory stimuli, and alphaMbeta2-deficient PMN displayed defective inflammatory functions.

91 in enhanced complement receptor 3-dependent PMN-ADCC against tumor cells.

92 f Ahr(-/-)mice recapitulated the derepressed PMN recruitment observed previously in Ido1(-/-)mice.

93 During PMN-mediated second organ injury, RvD2's protective acti

94 inflammation in diseases where dysregulated PMN influx is associated with host tissue damage.

95 d, Arg1, but not PD-L1, contributes to early PMN-driven T cell suppression in CF, likely hampering re

96 ce blocks chemotaxis and TEM while enhancing PMN-adhesive interactions with intestinal epithelia.

97 ounding host tissues, dysregulated/excessive PMN transmigration and resultant bystander-tissue damage

98 nclude that this TLR1 SNP leads to excessive PMN priming in response to cell stimulation.

99 y AT production and were activated to expand PMN numbers in proportion to S. aureus abundance in a ma

100 moval by PMN-MP-associated MMP-9 facilitates PMN trafficking across epithelial layers.

101 mor models, although the mechanisms favoring PMN-MDSC responses remain poorly understood.

102 ated the effect of an electric field to FeRh/PMN-PT heterostructures and report 8% change in the elec

103 The IL-8R knockout mice had fewer PMNs in the colon but the other variables we measured we

104 potent inhibition of wound closure following PMN-MP binding to IECs.

105 To analyze stimuli that are required for PMN activity during C. albicans infection in a situation

106 To establish an immune-regulatory role for PMN-derived LXA4 in dry eye, females were treated with L

107 s and reveal a context-specific capacity for PMNs to directly combat tumorigenesis.

108 we describe a surprising inhibitory role for PMNs in epithelial carcinogenesis.

109 derived GPs had an increased ability to form PMN-MDSCs; 3) tumor-derived GPs shared gene expression p

110 tudy highlights the importance of functional PMN, T-cell, and NK-cell immunity for the outcome of IA.

111 Furthermore, PMN-MP binding to intestinal epithelium in vitro in tran

112 rovide new insight into mechanisms governing PMN-induced tissue injury and implicate PMN-MPs and MPO

113 tor (PAF), a potent lipid mediator, in human PMNs.

114 HUVEC: PMN co-cultures were perfused for additional 15 minutes

115 ning PMN-induced tissue injury and implicate PMN-MPs and MPO as important regulators of cellular func

116 Our findings thus implicate PMN-MPs in PMN-mediated inflammation and epithelial dama

117 dase (MPO), which is abundantly expressed in PMN azurophilic granules and is used for microbial killi

118 nalysis was used to study mRNA expression in PMN from healthy subjects (normal PMN) and CGD PMN durin

119 r in integrin biology, with key functions in PMN trafficking during innate immunity.

120 abolic adaptation of Granulibacter growth in PMN included the upregulation of pyruvate dehydrogenase.

121 l loop preparations facilitated increases in PMN TEM.

122 nd induced an attached, spread morphology in PMN both at rest and in the presence of chemotactic stim

123 Our findings thus implicate PMN-MPs in PMN-mediated inflammation and epithelial damage, as obse

124 uman THP-1 macrophage-like cells, but not in PMN-HL60, was significantly higher than parental wild-ty

125 est that alphaMbeta2 plays a primary role in PMN inflammatory functions and regulates the anti-inflam

126 g M. tuberculosis infection, loss of Atg5 in PMNs can sensitize mice to M. tuberculosis.

127 ress response pathway were down-regulated in PMNs of diseased patients.

128 us promoting epithelial injury and increased PMN recruitment.

129 ted post-migratory PMN functions, increasing PMN phagocytosis and the surface mobilization of azuroph

130 emonstrating responses to oxygen-independent PMN antimicrobial systems.

131 red with wild-type PMNs and failed to induce PMN transmigration.

132 ally associated with amplified AMPhi-induced PMN migration into lung alveoli.

133 lial migration (P < 0.0001) and fMLP-induced PMN chemotaxis (ie, migration directionality and velocit

134 of this enzyme blocked S. pneumoniae-induced PMN transepithelial migration in vitro Genetic ablation

135 -/-) mice resulted in increased WNV-infected PMN infiltration and viral burden in the brain, which wa

136 roduction and migration capacity of infected PMNs, whereas GSH could restore these functions.

137 WNV neuroinvasion by recruiting WNV-infected PMNs into the brain.

138 ere proteinuria, few glomerulus-infiltrating PMN were found, leaving macrophages and, to a less exten

139 croparticles released by tissue infiltrating PMNs (PMN-MPs) serve as shuttles to protect and deliver

140 These tissue PMNs, unlike inflammatory PMNs, expressed a highly amplified LXA4 circuit and were

141 hway of myeloid differentiation to influence PMN-MDSC production has remained unknown.

142 In vitro, FGF23 inhibited PMN adhesion, arrest under flow, and transendothelial mi

143 y PMN of CGD patients (CGD PMN) and inhibits PMN apoptosis through unknown mechanisms.

144 Isolated PMN-MPs efficiently bound to IEC monolayers and induced

145 ARDS definition (n=10), in freshly isolated PMNs from age-matched and sex-matched healthy volunteers

146 We show that C-sep isolated PMNs show higher neutrophil elastase (NE) release follow

147 le of these macrophages but not the PD-L1(-) PMN in GN development and in inducing podocyte damage.

148 ted that blood polymorphonuclear leucocytes (PMNs) in ARDS are basally activated, and exhibit aberran

149 ion by reducing polymorphonuclear leukocyte (PMN) recruitment to the affected organs.

150 Neutrophil [polymorphonuclear leukocyte (PMN)] transepithelial migration (TEM) is a hallmark of i

151 Polymorphonuclear leukocytes (PMN) achieve an intermediate or primed state of activati

152 ation (TEM) of polymorphonuclear leukocytes (PMN) involves a carefully orchestrated dialog of adhesio

153 collected from polymorphonuclear leukocytes (PMN) selectively increased hNSC astrogliogenesis and pro

154 the influx of polymorphonuclear leukocytes (PMN; neutrophils).

155 Polymorphonuclear leukocytes (PMNs) are innate immune cells whose principal function i

156 er of necrotic polymorphonuclear leukocytes (PMNs) were observed in the lungs.

157 C5a receptors, polymorphonuclear leukocytes (PMNs), and the Nacht-, LRR-, and PYD-domains-containing

158 s, also called polymorphonuclear leukocytes (PMNs), extrude molecular lattices of decondensed chromat

159 overs 94.0% of polymorphonuclear leukocytes (PMNs), with up to 10(5) PMNs in clear diluted buffer fro

160 f neutrophils (polymorphonuclear leukocytes [PMN]), macrophages (MPhi), Langerin(+) dendritic cells (

161 n neutrophils (polymorphonuclear leukocytes [PMNs]) generate inflammatory responses within the joints

162 aphylococcus aureus infections, RvD2 limited PMN infiltration, enhanced phagocyte clearance of bacter

163 Major PMN effector mechanisms, including oxidative burst, rele

164 fy therapeutic targets aimed at manipulating PMN function and longevity.

165 cell detachment from the basement membrane, PMNs impeded early-stage tumor growth and retarded malig

166 tion of PMN membrane-derived microparticles (PMN-MPs) onto intestinal epithelial cells (IECs) during

167 , given its abundant expression on migrating PMN, Le(x) may be a rational target for modulating infla

168 IEC Dsg-2 serves as a barrier for migrating PMNs, and its removal by PMN-MP-associated MMP-9 facilit

169 e of terminal Le(x) regulated post-migratory PMN functions, increasing PMN phagocytosis and the surfa

170 a Helicobacter pylori mouse infection model, PMN infiltration into the gastric mucosa is dramatically

171 endotoxemia, we developed a new mouse model, PMN(DTR) mice, in which injection of diphtheria toxin in

172 important means of therapeutically modifying PMN-mediated vascular inflammation.

173 nog, and epithelial cell adhesion molecule), PMN infiltration, and clinical features of AH, such as h

174 rituximab in primary membranous nephropathy (PMN) have not been conducted.

175 Neutrophil (PMN) infiltration of the intestinal mucosa often leads t

176 monstrated the requirement for a neutrophil (PMN) subset expressing CD49d to drive development of pos

177 eleased during polymorphonuclear neutrophil (PMN) degranulation, and mediates dysregulation of vascul

178 r platelet and polymorphonuclear neutrophil (PMN) functions require specific thresholds of kindlin-3,

179 , WNV-infected polymorphonuclear neutrophil (PMN) infiltration and viral burden in brain of Opn (-/-)

180 thelium and on polymorphonuclear neutrophil (PMNs) after transepithelial migration into the alveolar

181 crophages and polymorphonuclear neutrophils (PMN) are important in inducing GN, as anti-CD11b and -IC

182 Polymorphonuclear neutrophils (PMN) have distinct phenotypes that drive inflammation bu

183 Because polymorphonuclear neutrophils (PMN) interaction with ECs generates reactive oxygen spec

184 ecruitment of polymorphonuclear neutrophils (PMN) to bacterial and fungal pathogens as well as to mod

185 es, including polymorphonuclear neutrophils (PMN), monocytes, and macrophages (MPhi).

186 The interaction of neutrophils (PMNs) and epithelial cells are requisite lines of commun

187 Polymorphonuclear neutrophils (PMNs) are innate effector cells with pivotal roles in pa

188 Polymorphonuclear neutrophils (PMNs) are innate immune system cells that play an essent

189 Polymorphonuclear neutrophils (PMNs) are largely considered to foster cancer developmen

190 rmine whether polymorphonuclear neutrophils (PMNs) are required for diarrhea for Salmonella colitis,

191 rafficking of polymorphonuclear neutrophils (PMNs) during inflammation critically depends on the beta

192 ecruitment of polymorphonuclear neutrophils (PMNs) from the bone marrow via the circulation and local

193 Polymorphonuclear neutrophils (PMNs) have previously been reported to mediate phagocyto

194 production by polymorphonuclear neutrophils (PMNs) of diabetic individuals in response to this bacter

195 thesized that polymorphonuclear neutrophils (PMNs), recruited massively into the CF airway lumen and

196 Pre-Metastatic Niches (PMNs) result from communications between primary tumors

197 In this paper, we study a FeGaB/NiTi/PMN-PT multiferroic heterostructure, which can be operat

198 Depressed lymph node PMN and LXA4 in females correlated with an increase in e

199 ression in PMN from healthy subjects (normal PMN) and CGD PMN during incubation with G. bethesdensis

200 Notably, PMN from donors with the SNP had higher surface levels o

201 ed by C5 cleavage, the cytotoxic activity of PMN in the presence of serum strongly depended on C5 cle

202 The enzymatic activity of PMN-MP-associated MPO was enhanced compared with soluble

203 lt demonstrates the potential application of PMN-PT nanostructures in energy harvesting, thus enrichi

204 We recently described UPEC attenuation of PMN trafficking to the urinary bladder through pathogen-

205 ic T-cell responses, and killing capacity of PMN against A. fumigatus were significantly decreased in

206 cribes a new mechanism whereby deposition of PMN membrane-derived microparticles (PMN-MPs) onto intes

207 tail of CD18 and is crucial for induction of PMN adhesion and postadhesion events, including adhesion

208 Importantly, localized microinjection of PMN-MPs into wounded colonic mucosa was sufficient to im

209 oteins are critical for initial migration of PMN out of the vasculature.

210 n parallel, CORM-401-dependent modulation of PMN chemotaxis, F-actin expression/distribution, and act

211 We investigated modulation of PMN-endothelial cell adhesive interactions by water-solu

212 ted into steps mediated by distinct pairs of PMN/endothelial interacting molecules.

213 he molecular details regarding regulation of PMN migration across mucosal epithelia are poorly unders

214 We focus on regulation of PMN number and function and the role of pore-forming alp

215 Stimulation of PMN with C5a led to upregulation of activated complement

216 Transition of PMN rolling to firm adhesion critically depends on Coro1

217 b, we observed that a mean of 50% and 75% of PMNs had taken a fraction of the dye from CLL B cells at

218 nt literature related to the contribution of PMNs to molding of the tissue microenvironment, with an

219 H levels and glutathione peroxidase (GPx) of PMNs after exposed to live B. pseudomallei.

220 Live imaging of PMNs showed that MRS2578 represses neutrophil migration

221 includes a robust inflammatory infiltrate of PMNs and macrophages.

222 imilar in both groups except for the lack of PMNs in the IL-8R knockout mice.

223 However, dysregulated migration of PMNs into mucosal epithelial tissues is characteristic o

224 e mechanism of transendothelial migration of PMNs.

225 In this group there was a reduced number of PMNs in the corneal stroma at 3 and 7 days of follow-up.

226 However, the role of PMNs in dry eye disease remains unexplored.

227 Thus, endotoxin-induced transmigration of PMNs was secondary to TRPM2-activated Ca(2+) signaling a

228 expression of C5a receptors was detected on PMN, whereas NK cells completely lacked expression.

229 sidues within glycan chains had no effect on PMN migration or adhesive interactions.

230 iferation, was not involved in its effect on PMN trafficking.

231 tric structure with Pt/Co/Ni/Co/Pt layers on PMN-PT substrate.

232 was increased surface expression of Le(x) on PMN after TEM, and blockade of terminal Le(x) regulated

233 okine-triggered beta2 integrin activation on PMNs by activating protein kinase A (PKA) and inhibiting

234 our data reveal that FGF23 acts directly on PMNs and dampens host defense by direct interference wit

235 downregulation of FGF receptor 2 (FGFR2) on PMNs rescued host defense in these mice.

236 od assays and in experiments in which MNC or PMN were combined with serum.

237 es, whereas no differences in ADCC by MNC or PMN were detected.

238 Ga nanomagnets delineated on a piezoelectric PMN-PT substrate.

239 2Nb1/2)O3-(y)Pb(Mg1/3Nb2/3)O3-(x)PbTiO3 (PIN-PMN-PT) crystals under high strain rate loading.

240 b(In1/2Nb1/2)O3-Pb(Mg1/3Nb2/3)O3-PbTiO3 (PIN-PMN-PT) relaxor ferroelectric single crystal.

241 The obtained results indicate that PIN-PMN-PT crystals became completely depolarized under 3.9

242 ticles released by tissue infiltrating PMNs (PMN-MPs) serve as shuttles to protect and deliver active

243 t monocytic (M)-MDSCs and polymorphonuclear (PMN)-MDSCs can be detected using several of the markers

244 or subsets, monocytic and polymorphonuclear (PMN).

245 SECs) and high numbers of polymorphonuclear (PMN) cells are regarded as indicative of a lower respira

246 itative reconstitution of polymorphonuclear (PMN), CD4, CD8, and natural killer (NK) cells against As

247 ith intense neutrophilic (polymorphonuclear; PMN) inflammation and high mortality.

248 CXCR7 antagonism reduced the most potent PMN chemoattractants CXCL1 and CXCL2/3.

249 (or inactive compound iCORM-401)-pretreated PMN for 5 minutes in the presence of 1.0 dyn/cm(2) shear

250 Pretreating PMN with CORM-401 did not suppress PMN adhesion to HUVEC

251 P-ribose polymerase in ECs of mice prevented PMN transmigration.

252 of the largest reported values for previous PMN-PT, PZT and ZnO nanostructures, respectively.

253 hat ligation of TLR2/1 or TLR2/6 would prime PMN.

254 Primed PMN have enhanced responsiveness to subsequent stimuli,

255 Patients with biopsy-proven PMN and nephrotic syndrome after 6 months of nonimmunosu

256 obal transcriptional profiles in highly pure PMNs from ventilated patients fulfilling the Berlin ARDS

257 ect any significant phagocytosis by purified PMNs of anti-CD20-opsonized CLL B cells, but could detec

258 h wild-type S. aureus enriched in AT reduced PMN recruitment and resulted in sustained bacterial burd

259 adhesion to HUVEC, but significantly reduced PMN transendothelial migration (P < 0.0001) and fMLP-ind

260 t mice revealed lower efficacies in reducing PMN infiltration, proinflammatory cytokine levels, and h

261 represents a potential target for regulating PMN trafficking and function in inflamed mucosa.

262 d understanding of the mechanisms regulating PMN transepithelial migration should provide insights in

263 t voltage of a lateral PNG built on a single PMN-PT nanobelt demonstrates the potential application o

264 c nanogenerator (PNG) is built on the single PMN-PT nanobelt, generating a maximum output voltage of

265 etreating PMN with CORM-401 did not suppress PMN adhesion to HUVEC, but significantly reduced PMN tra

266 rticularly L-kynurenine, directly suppressed PMN transepithelial migration and induced an attached, s

267 Surprisingly, PMN from only a subset of donors were primed in response

268 Given that PMN migration across mucosal epithelia is strongly corre

269 These findings support the hypothesis that PMN-MDSCs result from selective expansion of IRF8(lo) GP

270 Genotyping studies revealed that PMN responsiveness to Pam3CSK4 was enhanced by a common

271 We conclude that PMNs mediate mostly trogocytosis rather than phagocytosi

272 We found that PMNs from glibenclamide-treated diabetic individuals inf

273 However, recent data have suggested that PMNs, like macrophages, can also mediate trogocytosis.

274 (12-LOX), which is required to generate the PMN chemoattractant hepoxilin A3 (HXA3) from arachidonic

275 the metastable ferroelastic switching in the PMN-PT and an electrically rotatable local exchange bias

276 displayed as terminal glycan residues on the PMN surface blocks chemotaxis and TEM while enhancing PM

277 rection of the applied electric field on the PMN-PT substrate, which fully replaces the controllabili

278 DSC burden in tumor models, particularly the PMN-MDSC subset.

279 al killing, was found to be mobilized to the PMN surface and subsequently released in association wit

280 cyclic voltage applied perpendicular to the PMN-PT without a magnetic field, the local magnetization

281 act infections and further characterize this PMN subset in human subjects and mice.

282 Ab depletion of tissue PMN abrogated LXA4 formation in lymph nodes, as well as

283 specific regulation of LXA4-producing tissue PMN as a potential key factor in aberrant effector T cel

284 We discovered an LXA4-producing tissue PMN population in the corneal limbus, lacrimal glands, a

285 These tissue PMNs, unlike inflammatory PMNs, expressed a highly ampli

286 neutrophil recruitment, which contributes to PMN formation and metastasis.

287 to generate C1q and C3a; exposure of hNSC to PMN-synthesized concentrations of these complement prote

288 ficantly reduced Ca(2+) entry in response to PMN activation of TRPM2 in ECs.

289 inhibition of CXCR7 reduced transepithelial PMN migration by affecting the expression of adhesion mo

290 ow cytometric analysis of mutant Lkt-treated PMNs revealed the induction of necrosis.

291 in ECs via TRPM2 as compared with wild-type PMNs and failed to induce PMN transmigration.

292 rg1 and PD-L1 are dynamically modulated upon PMN migration into human airways, and, Arg1, but not PD-

293 ly released in association with PMN-MPs upon PMN activation and binding to intestinal epithelial cell

294 nly 292 (22%) were seen in healthy volunteer PMNs after exposure to rhGM-CSF, of which 216 showed the

295 volunteers (n=10), and in healthy volunteer PMNs exposed in vitro to recombinant human granulocyte-m

296 matched and gender-matched healthy volunteer PMNs treated with rhGM-CSF.

297 ranscriptomic overlap with healthy volunteer PMNs treated with rhGM-CSF.

298 d in ARDS PMNs relative to healthy volunteer PMNs.

299 nd subsequently released in association with PMN-MPs upon PMN activation and binding to intestinal ep

300 Upon interaction with PMN, G. bethesdensis altered the expression of ROS resis

301 were perfused for additional 15 minutes with PMN-free medium containing CORM-401/inactive CORM-401.

302 e-crystal (1 - x)Pb(Mg1/3Nb2/3)O3 - xPbTiO3 (PMN-PT) nanobelt with a superior piezoelectric constant