ライフサイエンスコーパス: human neutrophil

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

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

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

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

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

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

7 other inflammatory stimuli in both mouse and human neutrophils.

8 functions of paucimannosylation in activated human neutrophils.

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

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

11 d by Leishmania amazonensis promastigotes in human neutrophils.

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

13 e parental invasive strain after exposure to human neutrophils.

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

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

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

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

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

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

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

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

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

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

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

25 opsonin-dependent phagocytosis morphology of human neutrophils.

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

27 f propofol by competitively blocking FPR1 in human neutrophils.

28 hat specifically recognizes Stx1 and Stx2 in human neutrophils.

29 t and matched increase in circulating mature human neutrophils.

30 ne proteases stored in azurophil granules of human neutrophils.

31 mouse neutrophils and oxidant generation by human neutrophils.

32 regulation of opsonophagocytosis of AP53 by human neutrophils.

33 were used to detect binding between IgLC and human neutrophils.

34 d phagocytosis and killing of Pseudomonas by human neutrophils.

35 nib on functional responses of normal mature human neutrophils.

36 d NADPH oxidase-dependent NETs in vitro from human neutrophils.

37 plement-mediated opsonophagocytic killing by human neutrophils.

38 ich was associated with increased killing by human neutrophils.

39 iodontitis, we studied its interactions with human neutrophils.

40 0 in the range 22.2-32.2muM) from stimulated human neutrophils.

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

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

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

44 ese bacteria for opsonophagocytic killing by human neutrophils.

45 nduced both random and directed migration of human neutrophils.

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

47 y consistent with step aspiration studies of human neutrophils (5-30 Pa.s), our computational model p

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

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

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

51 details about extracellular trap release in human neutrophils activated by CPPD microcrystals.

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

53 and competitively inhibits the FPR1-induced human neutrophil activation.

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

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

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

57 Human neutrophils also expressed RORgammat and induced t

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

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

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

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

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

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

64 layer of the innate immune defense system of human neutrophils and catalyzes the production of strong

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

66 ed that Sp-D binds to SIRPalpha expressed on human neutrophils and differentiated neutrophil-like cel

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

68 In vitro, human neutrophils and eosinophils migrated toward supern

69 Migration of human neutrophils and eosinophils toward supernatants of

70 Using primary human neutrophils and genetically manipulated myeloid le

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

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

73 as been implicated in the oxidative burst in human neutrophils and is abundantly expressed in the lym

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

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

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

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

78 ate proinflammatory responses from mouse and human neutrophils and pulmonary cells.

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

80 phorylation of p47phox on selective sites in human neutrophils and suggest that p38 MAPK, ERK1/2, pro

81 to the uropods of chemoattractant-stimulated human neutrophils and T-cells and are involved in cell p

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

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

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

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

86 ch correlated with increased MRSA killing by human neutrophils and within neutrophil extracellular tr

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

88 1[D472N] podocytes accelerated chemotaxis of human neutrophils, and ABIN1[D472N] podocytes displayed

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

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

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

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

93 % CI, 1.08-3.4, P = .03), and volume of anti-human neutrophil antigen positive by granulocyte immunof

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

95 Human neutrophil apoptosis was assessed morphologically

96 nt/TRIF-dependent response and indicate that human neutrophils are able to recognize and respond to m

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

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

99 Human neutrophils are mediators of innate immunity and u

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

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

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

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

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

111 f did not induce NADPH oxidase activation in human neutrophils, but induced a dramatic increase of fM

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 he interaction between in vitro bacteria and human neutrophils by experiments and mathematical modeli

115 allergic contact sensitivity, as in isolated human neutrophils, C5L2 functions to suppress C5a-C5aR-m

116 In this study, we show that NETs released by human neutrophils can directly prime T cells by reducing

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

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

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

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

121 ort the identification of a subset of mature human neutrophils (CD11cbright/CD62Ldim/CD11bbright/CD16

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

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

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

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 ced platelet microbicidal protein (tPMP) and human neutrophil defensin-1 (hNP-1) from neutrophils.

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

131 Human neutrophils demonstrated similar LPS-induced chang

132 Mechanistic studies using human neutrophils demonstrated that inhibition of immune

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

134 Altogether, data demonstrate that human neutrophils, differently from either monocytes or

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

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

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

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

139 lished inhibitor of serine proteases such as human neutrophil elastase (HNE) and a NF-kappaB regulato

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

141 Human Neutrophil Elastase (HNE) is a serine protease tha

142 Human neutrophil elastase (HNE) is an attractive target

143 Human neutrophil elastase (HNE) is an important therapeu

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

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

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

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

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

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

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

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

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

153 st potent irreversible peptidyl inhibitor of human neutrophil elastase reported to date.

154 amino acids to explore the S1-S4 pockets of 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 In this study, we show that human neutrophils engulf CPPD crystals and form large am

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

160 These forms are produced by activated human neutrophils ex vivo, are biologically active in vi

161 We report that human neutrophils exposed to pregnancy hormones progeste

162 Here, human neutrophils exposed to uniform shear stress (0.1-4

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

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

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

166 ploited mice and cell lines expressing these human neutrophil FcgammaRs to demonstrate that FcgammaRI

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

168 Human neutrophils fed CA-MRSA lacked phosphorylated RIPK

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

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

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

172 Human neutrophils form extracellular traps during M. tub

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

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

175 Human neutrophil gelatinase associated lipocalin (NGAL)

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

177 Human neutrophils generate MPs at a threshold of approxi

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

179 oteolysis of ADAM10 and ADAM17 substrates in human neutrophil granulocytes, endothelial cells and mur

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 inhibits Ca(2+) signalling and chemotaxis in human neutrophils, illustrating the potential for pharma

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

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

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

187 Human neutrophils in bMFA preferentially adhered to acti

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

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

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

191 Adhesion of human neutrophils in the presence of whole serum was sig

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

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

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

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

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

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

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

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

202 re-dependent heat treatment of serum affects human neutrophil interactions with "target" particles of

203 Here we analyze human neutrophil interactions with interleukin (IL)-1bet

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

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

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

207 diated adhesion and chemotactic migration of human neutrophil-like differentiated HL-60 cells, mAbp1

208 t (S133A) resulted in a decreased ability of human neutrophil-like PLB-985 cells to generate inflamma

209 In humans, neutrophils, mast cells, basophils, and eosinoph

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

211 th our in vivo findings, we demonstrate that human neutrophils migrate toward the supernatant of IL-3

212 stigate how cell-cell interactions influence human neutrophil migration and surface marker expression

213 f chemoattractant enabled the measurement of human neutrophil migration on a cell monolayer to probe

214 ulture chamber, enabled the investigation of human neutrophil migration patterns in the presences of

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

216 everal chemokines, which effectively induced human neutrophil migration.

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

218 m I. ricinus did not affect NET formation by human neutrophils or its stability.

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

220 estigated the interaction of polymyxin B and human neutrophil peptide (HNP-1) with the human pathogen

221 The human neutrophil peptide 1 (HNP-1) is known to block the

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

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

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 ers of the human alpha-defensin family: four human neutrophil peptides, including HNP1, and two enter

227 Human neutrophils (polymorphonuclear leukocytes [PMNs])

228 lity of the pathogen to avoid destruction by human neutrophils (polymorphonuclear leukocytes [PMNs]),

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

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

231 In human neutrophils, PSMs exert their function by binding

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

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

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

235 Human neutrophils release IL-1beta and IL-8 in response

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

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

238 ochemistry of these modifications in primary human neutrophils remains relatively unstudied.

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

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

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

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

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

244 Endogenous inhibitors of human neutrophil serine proteases preferentially inhibit

245 Human neutrophils specifically bind Stx through TLR4, th

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

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

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

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

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

251 function can be accomplished by a subset of human neutrophils that can be systemically induced in re

252 erpinB1 from the cytoplasm to the nucleus of human neutrophils that is coincident with or preceding e

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

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

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

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

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

258 ifungal defense, we studied the responses of human neutrophils to clinical isolates of both C. albica

259 Our goal is to describe the capacity of human neutrophils to control highly virulent B. pseudoma

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

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

262 RK5, and NF-kappaB promote the attachment of human neutrophils to lung microvascular EC that were pre

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

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

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

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

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

268 or alphaMbeta2 integrin-mediated adhesion of human neutrophils under shear and static conditions and

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

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

271 In this study, human neutrophil uptake of GFP-expressing F. tularensis

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

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

274 re, we found that electropermeabilization of human neutrophils, used as a separate means to create po

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

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

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

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

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

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

281 Using both murine model systems and in vitro human neutrophils, we found that NADPH oxidase produced

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 In agreement with our in vivo data, isolated human neutrophils were cytotoxic to HepG2 cells when coc

286 Primary human neutrophils were exposed to supernatants prepared

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 nd that NETs are produced in vitro by primed human neutrophils when challenged with anti-HNA-3a antib

291 r phagocytosis of opsonized F. tularensis by human neutrophils, whereas CR3 and CR4 (CD11c/CD18) medi

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

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

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

295 However, the receptor that recognizes Stx in human neutrophils, which do not express Gb3Cer, has not

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

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