ライフサイエンスコーパス: human neutrophil

1 iodontitis, we studied its interactions with human neutrophils.

2 0 in the range 22.2-32.2muM) from stimulated human neutrophils.

3 s of this natural product on the function of human neutrophils.

4 bits phagocytic killing of M. catarrhalis by human neutrophils.

5 ese bacteria for opsonophagocytic killing by human neutrophils.

6 ntial to trafficking and immune functions of human neutrophils.

7 nduced both random and directed migration of human neutrophils.

8 appaB phosphorylation and IL-8 production in human neutrophils.

9 ing that F. alocis increases chemokinesis in human neutrophils.

10 -mediated necroptotic death of GM-CSF-primed human neutrophils.

11 he susceptibility of S. aureus to killing by human neutrophils.

12 dation was further carried out in vitro with human neutrophils.

13 m and for the lamellipod-driven migration of human neutrophils.

14 tial to import LL-37 released from activated human neutrophils.

15 lease of Ca(2+) from intracellular stores in human neutrophils.

16 other inflammatory stimuli in both mouse and human neutrophils.

17 functions of paucimannosylation in activated human neutrophils.

18 gaps in our understanding of the behavior of human neutrophils.

19 d reduced interleukin-8 (IL-8) production in human neutrophils.

20 d by Leishmania amazonensis promastigotes in human neutrophils.

21 on murine splenocytes, purified B cells, and human neutrophils.

22 ct (ANE) inhibits the phagocytic activity of human neutrophils.

23 ginosa induce DNA, MPO, and HNE release from human neutrophils.

24 hloramines, MPO/H2O2/chloride, and activated human neutrophils.

25 ses, induce the release of NETs from primary human neutrophils.

26 cal for the cytotoxicity of S. aureus toward human neutrophils.

27 e early and late response to fMLF and TNF in human neutrophils.

28 rophages enhanced efferocytosis of apoptotic human neutrophils.

29 c target to block the effect of LukAB toward human neutrophils.

30 xidase components p47(PHOX) and p22(PHOX) in human neutrophils.

31 xin that contributes to S. aureus killing of human neutrophils.

32 mice; juvenile Sprague-Dawley rats, primary human neutrophils.

33 opsonin-dependent phagocytosis morphology of human neutrophils.

34 turn, IL-18 is able to stimulate NETosis in human neutrophils.

35 we show that osc-modCs are also prevalent in human neutrophils.

36 in mice and in ex vivo models using primary human neutrophils.

37 2 fragment (Slit2-S) is a chemorepellent for human neutrophils.

38 n of ROS as part of its survival strategy in human neutrophils.

39 rophil-like HL-60 (dHL-60) cells, or primary human neutrophils.

40 ose responsively reduce LTB(4) production in human neutrophils.

41 rototypic type 2 cytokines IL-4 and IL-13 on human neutrophils.

42 ich was associated with increased killing by human neutrophils.

43 phil extracellular traps (NETs) in mouse and human neutrophils.

44 e parental invasive strain after exposure to human neutrophils.

45 r traps (NETs) in a size-dependent manner by human neutrophils.

46 Inflammatory conditions can profoundly alter human neutrophils, a leukocyte subset generally viewed a

47 so oxidized in ADAMTS13 exposed to activated human neutrophils, accompanied by reduced enzyme activit

48 a substantial fraction of beta2 integrins on human neutrophils acquire an unexpected E(-)H(+) conform

49 eration, elastase release, and chemotaxis in human neutrophils activated by fMLF.

50 mans, were similarly reduced by AAT or rAAT; human neutrophils adhering to endothelial cells were dec

51 IL-4 receptor signaling in human neutrophils affects several neutrophil effector fu

52 PP2A activation was assessed in human neutrophils, airway epithelial cells, and peripher

53 s to atherogenesis, we studied the effect of human neutrophil alpha-defensins on low density lipoprot

54 Human neutrophils also expressed RORgammat and induced t

55 cose-promoted chemotaxis of freshly isolated human neutrophils also was blocked by PPTN.

56 In this article, we show that human neutrophils altered their expression of IL-20R cha

57 e hypothesized that the kinetics of isolated human neutrophil and eosinophil migration through major

58 resulted in weak killing of the bacteria by human neutrophils and a corresponding high death rate of

59 Screening of 367 kinase inhibitors in human neutrophils and a zebrafish tail fin injury model

60 itro assay in which the interactions between human neutrophils and A. fumigatus were observed in real

61 om antimicrobial reactive oxygen produced by human neutrophils and activated macrophages.

62 luorescein isothiocyanate (FITC) staining of human neutrophils and anti-Dectin-1-FITC staining of mou

63 nt regulator of proinflammatory signaling in human neutrophils and demonstrated that intratracheal in

64 esolution time-lapse microscopy of mouse and human neutrophils and differentiated HL-60 neutrophil-li

65 in vitro resulted in decreased chemotaxis of human neutrophils and diminished calcium signaling in mo

66 In vitro, human neutrophils and eosinophils migrated toward supern

67 Migration of human neutrophils and eosinophils toward supernatants of

68 titate RNA for H1 histone subtypes in mature human neutrophils and identify citrulline residues by li

69 stimulation of oxygen radical production in human neutrophils and increasing tissue damage during sk

70 LLO can enhance the phagocytic efficiency of human neutrophils and is unable to protect L. monocytoge

71 We demonstrated that PAT1 is expressed in human neutrophils and monocytes and colocalizes with p22

72 measuring tractions generated by both single human neutrophils and multicellular monolayers of Madin-

73 nisms of relevance to the cross talk between human neutrophils and NK cells and its potential role in

74 are demonstrated to inhibit the staining of human neutrophils and of mouse macrophages by fluorescen

75 on the spontaneous chemiluminescence (CL) of human neutrophils and only mild effect on PMA-activated

76 genesis, explains the toxin's tropism toward human neutrophils and other phagocytes, and provides a c

77 y aspects of the interaction between primary human neutrophils and S. aureus biofilms and provides in

78 erns and regulation of SGK family members in human neutrophils and shown that inhibition of SGK activ

79 ocalin-2 (LCN2) was originally isolated from human neutrophils and termed neutrophil gelatinase-assoc

80 er, Tie2 expression has been demonstrated on human neutrophils and the observation that neutrophils m

81 Functional studies of human neutrophils and their transfusion for clinical pur

82 ns were also separately purified from normal human neutrophils and used to reconstitute chromatin usi

83 cells, a high level of opsonophagocytosis by human neutrophils, and a very low death rate of mice inf

84 1[D472N] podocytes accelerated chemotaxis of human neutrophils, and ABIN1[D472N] podocytes displayed

85 e content and NET formation also occurred in human neutrophils, and correlated with the incidence and

86 e was limited binding and uptake of ST258 by human neutrophils, and correspondingly, there was limite

87 ues, fMLF peptide-induced oxidative burst in human neutrophils, and cytokine production in human peri

88 t leukotriene B(4) (LTB(4)), specifically in human neutrophils, and this correlated with a reduction

89 sis inhibited the basal respiratory burst in human neutrophils, and those generated from PR3-expressi

90 dies to human lymphocyte antigen (HLA)-A2 or human neutrophil antigen (HNA)-3a was filtered, and immu

91 attributed to passive infusion of HLA and/or human neutrophil antigen antibodies present in transfuse

92 Human neutrophil antigen-3a (HNA-3a) antibodies containe

93 Human neutrophil apoptosis was assessed morphologically

94 Human neutrophils are critical for the innate immune res

95 her, these results suggest that proteases in human neutrophils are dispensable for protection against

96 omotypic aggregation nor NETosis occurs when human neutrophils are exposed either to immobilized fung

97 Human neutrophils are isolated from blood freshly drawn

98 Human neutrophils are mediators of innate immunity and u

99 Yet because human neutrophils are not amenable to many biological te

100 ion and functionality of the inflammasome in human neutrophils are poorly defined.

101 i induces N1-like subtype differentiation of human neutrophils as indicated by profound nuclear hyper

102 We here use human neutrophils as uniquely capable biodetectors to ma

103 yl-leucyl-phenylalanine induced spreading of human neutrophils as well as activation of the GTPase Ra

104 Moreover, Stx interact with human neutrophils, as experimentally demonstrated in vit

105 The present study demonstrates that human neutrophils assume Ag cross-presenting functions a

106 hat alpha defensins, released from apoptotic human neutrophils, augmented the antimicrobial capacity

107 serum DPPIV concentration cause movement of human neutrophils away from the higher concentration of

108 fference in ROS production levels in primary human neutrophils between these backgrounds can be attri

109 In motile, rapidly deforming cells such as human neutrophils, bulk cytoplasmic flow couples cell de

110 We found that SLE- and RA-IgG both bound human neutrophils but differentially regulated neutrophi

111 ro ANCA did not activate NF-kappaB in primed human neutrophils, but ANCA-stimulated primed neutrophil

112 Importantly, CD177(pos) human neutrophils, but not CD177(neg) neutrophils, showe

113 ted macrophages before infections shows that human neutrophils, but not macrophages, are key immune c

114 Here, we demonstrate that freshly isolated human neutrophils can function as antigen-presenting cel

115 HL-60 neutrophil-like cell line and primary human neutrophils can migrate against the direction of f

116 isting of a polarized mucosal epithelium and human neutrophils can provide a versatile model of trans

117 Human mast cell chymase (HC) and human neutrophil cathepsin G (hCG) show relatively simil

118 -associated molecular pattern beta-glucan by human neutrophils causes rapid (</= 30 min) homotypic ag

119 While Staphylococcus aureus accelerates human neutrophil cell death, the underlying host- and pa

120 y, we explored transcriptional complexity in human neutrophils, cells generally regarded as nonspecif

121 SLURP1 also suppressed the primary human neutrophil chemotaxis, and interaction with HUVEC.

122 CXCL2 and CXCL8 concentrations for mouse and human neutrophil chemotaxis, respectively.

123 a significantly larger respiratory burst in human neutrophils compared with control MVs.

124 2rg(-/-) mice was reduced in IL-4-stimulated human neutrophils compared with control values.

125 ocytes and to promote chemotaxis of isolated human neutrophils confirmed these as FFA2 processes medi

126 WASP depletion from human neutrophils confirms that both proteins are involv

127 In this study, we demonstrated that human neutrophils constitutively express Sema3E high-aff

128 Many elements of human neutrophil defenses appear redundant, and so the e

129 of the present study include: 1) to localize human neutrophil defensin-1 (HNP-1) through HNP-3 in gin

130 Human neutrophils demonstrated similar LPS-induced chang

131 Mechanistic studies using human neutrophils demonstrated that inhibition of immune

132 in, a fluorescent analog of fMLF, to FPR1 in human neutrophils, differentiated THP-1 cells, and FPR1-

133 We further show that human neutrophils display a higher cytotoxic activity ag

134 from Nuc-containing N. gonorrhoeae degraded human neutrophil DNA and NETs.

135 We further show that healthy human neutrophils do not complete mitophagy upon inducti

136 bate, it is now largely accepted that normal human neutrophils do not synthetize tissue factor, the i

137 ndant due to their cytotoxic activity toward human neutrophils, each toxin displays varied species an

138 wo typical inflammatory salivary biomarkers, Human Neutrophil Elastase (HNE) and Cathepsin-G, was con

139 Human neutrophil elastase (HNE) is an attractive target

140 s of elafin and cathelicidin, and the enzyme human neutrophil elastase (HNE) were measured in over 1,

141 d antibodies that inhibit bovine trypsin and human neutrophil elastase (HNE) with low nanomolar affin

142 hil serine proteases, proteinase 3 (PR3) and human neutrophil elastase (HNE), are considered as targe

143 ranule components, myeloperoxidase (MPO) and human neutrophil elastase (HNE), are inflammatory marker

144 selection of 2'-F purine aptamers that bind human neutrophil elastase (HNE).

145 y and optimization of covalent inhibitors of human neutrophil elastase (hNE).

146 sylation fine-tunes the RCL cleavage rate by human neutrophil elastase (NE) and Pseudomonas aeruginos

147 issociation constant with its primary target human neutrophil elastase (NE) in lipoprotein-containing

148 s display low cytotoxicity in vitro, inhibit human neutrophil elastase activity, and inhibit the migr

149 nt (TCP96), are produced through cleavage by human neutrophil elastase and aggregate lipopolysacchari

150 Here, we show that human neutrophil elastase cleaves thrombin, generating 1

151 ensive biological characterization of potent human neutrophil elastase inhibitors, which offer revers

152 large hydrophobic 2' substituents that bind human neutrophil elastase or the blood coagulation prote

153 amino acids to explore the S1-S4 pockets of human neutrophil elastase.

154 ls to restore specificity against trypsin or human neutrophil elastase.

155 rimary granule enzymes, myeloperoxidase, and human neutrophil elastase.

156 8-Hydroxy-2'-deoxyguanosine (8-OHdG) and human neutrophil elastase/alpha1-proteinase inhibitor (H

157 These data were translated by assessing human neutrophil-endothelial interactions under flow: PD

158 aphylococcus aureus targeting and killing of human neutrophils ex vivo and is produced in the setting

159 xidative stress in vitro and from killing by human neutrophils ex vivo.

160 We report that human neutrophils exposed to pregnancy hormones progeste

161 In summary, these studies show that human neutrophils express key components of the inflamma

162 Here we demonstrate that highly purified human neutrophils express key components of the NOD-like

163 Human neutrophils expressed both types of IL-4 receptors

164 Here we show that primary human neutrophils expressed immunoglobulin-like transcri

165 eported that necrostatin-1 inhibits lysis of human neutrophils fed CA-MRSA and attributed the process

166 Human neutrophils fed CA-MRSA lacked phosphorylated RIPK

167 In vitro, human neutrophils fed CA-MRSA lyse by an unknown mechani

168 s us to estimate the c/j0-threshold at which human neutrophils first detect nearby beta-glucan surfac

169 found that, unlike PVL, LukGH did not prime human neutrophils for increased production of reactive o

170 Human neutrophils form extracellular traps during M. tub

171 protein-coupled receptor to be described on human neutrophils, formyl peptide receptor 1 (FPR1), is

172 has immunomodulatory properties that protect human neutrophils from injury and provides insight into

173 olated mouse neutrophils from bone marrow or human neutrophils from peripheral blood were assessed in

174 Human neutrophils from peripheral blood were assessed wi

175 In conclusion, we show that PGE2-G inhibits human neutrophil functions through its hydrolysis into P

176 Human neutrophil gelatinase associated lipocalin (NGAL)

177 In human neutrophil gene array studies, we show that PKA ac

178 Human neutrophils generate MPs at a threshold of approxi

179 piratory burst oxidase homolog (Rboh) of the human neutrophil gp91phox.

180 eutrophil-fungus interactions and found that human neutrophils have a limited ability to migrate towa

181 Human neutrophils have traditionally been thought to hav

182 enoted ARM1, that inhibits LTB4 synthesis in human neutrophils (IC50 of approximately 0.5 muM) and co

183 were confirmed in both Dictyostelium and in human neutrophils in a directed EZ-TAXIscan chemotaxis a

184 rrode the survival-inducing effect of LPS in human neutrophils in an AnxA1-dependent manner.

185 We found that Mtb induces necrosis of human neutrophils in an ESX-1-dependent manner, and neut

186 Human neutrophils in bMFA preferentially adhered to acti

187 kocytes-1 (SIRL-1) attenuates NET release by human neutrophils in response to distinct triggers, incl

188 the release of reactive oxygen species from human neutrophils in response to P. falciparum blood-sta

189 tions for the inhibitory role of siglec-9 on human neutrophils in sepsis and acute lung injury.

190 killing of serum-opsonized M. catarrhalis by human neutrophils in vitro.

191 n associated lipoprotein, induced NETosis in human neutrophils in vitro.

192 also more susceptible than BG2 to killing by human neutrophils in vitro.

193 h higher resistance to nonopsonic killing by human neutrophils in vitro.

194 ated proteins of the azurophilic granules of human neutrophils including myeloperoxidase (MPO), azuro

195 nhances several pro-inflammatory pathways in human neutrophils, including chemotaxis, phagocytosis an

196 man airway drives changes in the behavior of human neutrophils, including increasing activation marke

197 AG825 significantly accelerated apoptosis of human neutrophils, including neutrophils from people wit

198 The blocking ability of human neutrophils increased to 85.1% when they were stim

199 ng that IL-4 receptor signaling in mouse and human neutrophils inhibited their migration toward CXCL2

200 r with planktonic (non-biofilm) C. glabrata, human neutrophils initially phagocytose the yeast and su

201 f eicosanoid that both stimulates and primes human neutrophil integrin (Mac-1) expression, in respons

202 uring platelet activation that can stimulate human neutrophil integrin expression.

203 In this review, we discuss how human neutrophils interact with both the symbiotic and t

204 omote the early epithelial transmigration of human neutrophils into the airspace in response to A. fu

205 utants displayed increased susceptibility to human neutrophil killing and reduced virulence in a muri

206 xtract (CSE) exposure enhances resistance to human neutrophil killing, but this increase in pathogeni

207 hanisms of Aspergillus conidia and hyphae by human neutrophils, leading to a comprehensive insight in

208 njury caused by mitochondrial extract-primed human neutrophils, leading to the conclusion that NADPH

209 MRSA USA300_FPR3757 mediated differentiated human neutrophil-like cells (dHL60) motility arrest by i

210 AP53 and M23ND display similar resistance to human neutrophil-mediated phagocytosis, which results in

211 human macrophages, but its ability to induce human neutrophil migration is substantially lower compar

212 ry capacity, whereas ELMO1 knockdown reduces human neutrophil migration to chemokines linked to arthr

213 The antimigratory effect of Sema3E on human neutrophil migration was associated with suppressi

214 f activation-mediated mechanisms that impair human neutrophil migration.

215 significantly more effective in attenuating human neutrophil migration.

216 everal chemokines, which effectively induced human neutrophil migration.

217 nding chemokine receptors CXCR1 and CXCR2 on human neutrophils on IL-4 or IL-13 stimulation in vitro.

218 timicrobial proteins released from activated human neutrophils, on clot formation in vitro and in viv

219 ies (ROS and RNS, respectively), to modulate human neutrophils' oxidative burst and to protect Caco-2

220 the most abundant neutrophil alpha defensin, Human Neutrophil Peptide 1 (HNP1).

221 t immune sources: neutrophil alpha-defensin (human neutrophil peptide 1 [hNP-1]), cutaneous beta-defe

222 tive oxygen species production, and released human neutrophil peptide levels, and attenuated neutroph

223 dentify short antimicrobial motif (Pep-H) of human neutrophil peptide-1 (HNP-1) and explore its antim

224 ited to the airway of diseased lung, release human neutrophil peptides (HNP1-4) that are cytotoxic to

225 Here, we show that human neutrophil peptides (HNPs) released from activated

226 fluence of smoking on cathelicidin LL-37 and human neutrophil peptides 1 through 3 (HNP 1-3) levels i

227 r, TC-derived soluble mediators modulate the human neutrophil phenotype.

228 K. pneumoniae to killing by freshly isolated human neutrophils, platelets, and serum when complement

229 ypdA mutant exhibited decreased survival in human neutrophils (PMNs) as compared with the parent, wh

230 Human neutrophils (polymorphonuclear leukocytes [PMNs])

231 A coculture of human neutrophils preactivated with 50 uM NA and B. thai

232 Here, however, human neutrophil preexposure to uniform shear stress (0.

233 onclusion, we are the first to document that human neutrophils produce, store and, upon activation, s

234 ablish CD117(+)CD71(+) eNeP as the inceptive human neutrophil progenitor and propose a refined model

235 cytometry to show that two recently defined human neutrophil progenitor populations contain a homoge

236 nsfers, indicate that eNePs are the earliest human neutrophil progenitors.

237 Upon microbial exposure, however, human neutrophils rapidly (<3 h) repositioned the ensemb

238 However, the mechanisms by which human neutrophils recognize and kill Aspergillus are poo

239 BMP9 pretreatment synergistically increases human neutrophil recruitment to LPS-stimulated human end

240 f TLR4 and VCAM-1 and inhibited BMP9-induced human neutrophil recruitment to LPS-stimulated human end

241 In this article, we show that human neutrophils release large amounts of neutrophil ex

242 Primary human neutrophils released NETs after exposure to N. gon

243 ex vivo testing of the beta2 AR response in human neutrophils represents a robust tool with good sig

244 cated that monocytic THP-1 cells and primary human neutrophils require ADAM10 but not ADAM17 for effi

245 alized as well as primary murine B cells and human neutrophil, respectively, resulted in decreased FL

246 Our previous work in human neutrophils revealed a unique role for C5L2 in neg

247 Fluorescence imaging of individual human neutrophils revealed that neutrophils treated with

248 Endogenous inhibitors of human neutrophil serine proteases preferentially inhibit

249 Human neutrophils specifically bind Stx through TLR4, th

250 tidase (NEP) activity and other functions of human neutrophils, such as elastase, MMP-9 and IL-8 prod

251 OX-1 is presented that can activate or prime human neutrophils, suggesting a role in innate immunity

252 ent chemoattractants in Dictyostelium and in human neutrophils, suggesting an evolutionarily conserve

253 We demonstrate that CD11b renders human neutrophils susceptible to LukAB-mediated killing

254 In this article, we report that in human neutrophils, TAK1 can also be activated by differe

255 s study, we describe an apoptotic pathway in human neutrophils that is triggered via the surface mole

256 rotein expressed by a variable proportion of human neutrophils that mediates surface expression of th

257 s enhanced capacity to circumvent killing by human neutrophils, the primary cellular defense against

258 Stx interact with human neutrophils through their A chain, since these leu

259 le, we demonstrate that in vitro exposure of human neutrophils to C5a significantly increased pHi by

260 The ability of human neutrophils to clear newly attached Staphylococcus

261 it2 blocked the capture and firm adhesion of human neutrophils to inflamed vascular endothelial barri

262 n also significantly reduced cytotoxicity in human neutrophils to levels observed in cells following

263 currently unsolved issue on the capacity of human neutrophils to produce IL-10.

264 e ICs containing Sm/RNP, an RNA Ag, activate human neutrophils to produce reactive oxygen species (RO

265 endent kinase inhibitor (R)-roscovitine into human neutrophils to promote apoptosis in vitro.

266 ased the level of survival after exposure to human neutrophils to that for the parental invasive stra

267 The contribution of human neutrophils to the protection against fungal infec

268 pneumoniae mutant was impaired in triggering human neutrophil transepithelial migration in vitro.

269 nstrate that MIF decreases the PC barrier to human neutrophil transmigration by increasing intercellu

270 mily kinases (SFKs) in these responses using human neutrophils treated with inhibitory compounds or m

271 In the current study, we report that human neutrophils undergo necroptosis after exposure to

272 CD11b was modified neither in murine nor in human neutrophils upon alpha2-agonist treatment.

273 B21, PIP5K1C90, and PM PtdIns4P in mouse and human neutrophils upon integrin stimulation.

274 ed genetic defects, we provide evidence that human neutrophils use 2 distinct and independent phagoly

275 We have observed that human neutrophils use large filopodia as cellular tentac

276 minidase A and the azurophilic marker MPO in human neutrophils using immunocytochemistry.

277 IVIG can alter the viability of human neutrophils via agonistic antibodies to Fas and Si

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

279 ns but not normal immunoglobulins stimulated human neutrophils via LILRA2.

280 Furthermore, specific binding of rhAPC to human neutrophils via VLA-3 was inhibited by an antagoni

281 f Candida glabrata following phagocytosis by human neutrophils was performed, and results were compar

282 Using human neutrophils, we identified a 15-kDa TREM-1 isoform

283 In the current study, human neutrophils were activated in vitro with immobiliz

284 ived podocytes, and interaction with primary human neutrophils were also assessed.

285 Primary human neutrophils were exposed to supernatants prepared

286 Primary human neutrophils were exposed to the pneumococcal strai

287 Elastase(+) human neutrophils were maximal during menstruation; Ly6G

288 In this study, human neutrophils were stimulated to produce NETs in pla

289 Rat carotid body chemosensitive cells, and human neutrophils, were treated with TLR agonists to act

290 ed regulation of CXCR1 surface expression on human neutrophils, whereas matrix metalloproteases are d

291 ut not Fc fragments of IVIG induced death of human neutrophils, whereas neither of these IVIG fragmen

292 imilarly induced cytokine-dependent death in human neutrophils, whereas they had no effects on the su

293 creased adhesive phenotype, and treatment of human neutrophils with a CB(2) agonist blocked their end

294 Treatment of human neutrophils with IL-4 suppressed HIF-1alpha-depend

295 Interaction of human neutrophils with MSU crystals was evaluated by hig

296 by freshly isolated, PMA-stimulated primary human neutrophils with primary human monocyte-derived ma

297 Here, we report that the treatment of human neutrophils with recombinant a2NTD leads to neutro

298 biofilm system to monitor the interaction of human neutrophils with staphylococcal biofilms and demon

299 Pretreatment of human neutrophils with tamoxifen boosts neutrophil bacte

300 nhibit exocytosis of azurophilic granules in human neutrophils without affecting other important inna