ライフサイエンスコーパス: fMLP

1 fMLP and IC each initiate a rapid transient rise in [Ca(

2 fMLP immobilized onto the surface of a bead interacts wi

3 fMLP induced phosphorylation of c-Cbl that was sustained

4 fMLP induced phosphorylation of MAPK isoforms, ERK1/2 an

5 fMLP initiated normal Ca(2+)-signal, activation of the e

6 fMLP reduced PMN migration into fibrin gels and allowed

7 fMLP stimulation also increased cPLA(2) activity in eosi

8 fMLP stimulation for 18 h was also found to induce modes

9 fMLP stimulation resulted in a p38 MAPK-dependent increa

10 fMLP uptake by colonic cells expressing GFP-hPepT1 speci

11 fMLP-induced RB of PMN from patients with decompensated

12 fMLP-induced shape changes were more pronounced in circu

13 eometer in the presence of the PMN activator fMLP.

14 Additionally, fMLP-stimulated phosphorylation of protein kinase B and

15 s suggest that deltaT does not likely affect fMLP receptor-mediated signaling or store depletion-indu

16 whereas none of the Hsp27 proteins affected fMLP-stimulated or TNF-alpha-stimulated exocytosis or ac

17 PMA-stimulated neutrophils without affecting fMLP-induced Ca(2+) mobilization and cell viability.

18 e functional expression of the high-affinity fMLP receptor.

19 o plasma membrane-containing fractions after fMLP stimulation.

20 gelatinase granule fractions increased after fMLP stimulation in a p38 MAPK-dependent manner.

21 The nonselective Fpr agonists, fMLP (6 mug/mouse, approximately 17 nmol) and AnxA1(Ac2-

22 Cells exposed to ambient fMLP concentrations near the constant of dissociation (K

23 transendothelial migration (P < 0.0001) and fMLP-induced PMN chemotaxis (ie, migration directionalit

24 osphorylation caused by IL-5, eotaxin-1, and fMLP.

25 for transmigration mediated by IL-1beta and fMLP (integrin-dependent), but not IL-8 (integrin-indepe

26 ed neutrophil chemotaxis induced by IL-8 and fMLP but decreased chemokinesis for neutrophils.

27 tional persistence in a gradient of IL-8 and fMLP.

28 , chemokine C-X-C motif ligands 2 and 8, and fMLP) and competing gradients of all pairwise combinatio

29 NH(2) and PUGNAc increase both the basal and fMLP-induced activity of a central mediator of cellular

30 of F-actin levels/cellular distribution and fMLP-induced phosphorylation of PAK1/2 and ERK/JNK MAPK

31 urst upon stimulation with phorbol ester and fMLP, Gsr-deficient neutrophils displayed a very transie

32 ated with platelet-derived growth factor and fMLP, respectively, was also detectable at picomole sens

33 Treatment of neutrophils with fibrinogen and fMLP resulted in minimal changes in the steady state lev

34 e relative effects of capillary geometry and fMLP on neutrophil transit time are presented as a simpl

35 e relative effects of capillary geometry and fMLP-stimulation on transit time.

36 s failed to translocate up the IL-8, KC, and fMLP gradients.

37 res of bacterial products/components LPS and fMLP behave synergistically in the induction of inflamma

38 f inflammation by bacterial products LPS and fMLP represents an important pathogenic mechanism during

39 ways in regulating PMN activation by LPS and fMLP.

40 Decreased LPS- and fMLP-induced phosphorylation of p38 MAPK in both IRAK4-

41 hemotaxins such as leukotriene B4 (LTB4) and fMLP is unknown.

42 FPR is not associated with lipid rafts, and fMLP-induced signaling does not require lipid raft integ

43 paired O(2)( ) generation by LPS-treated and fMLP-activated IRAK4-deficient PMN that correlated with

44 colocalized with F-actin in unstimulated and fMLP-stimulated neutrophils, whereas phosphorylated Hsp2

45 grating in the presence of uniformly applied fMLP and leukemic HSB2 T lymphocytes migrating on ICAM-1

46 neutrophil migration towards ligands such as fMLP shows that, although PtdIns(3,4)P(2) and PtdIns(3,4

47 eutrophil exposure to 15-epi-LXA4 attenuated fMLP triggered PKCbetaII phosphorylation and its interac

48 , P-Rex1 deficiency significantly attenuated fMLP-induced F actin formation and superoxide production

49 inhibitory peptide significantly attenuated fMLP-stimulated, but not PMA-stimulated, superoxide rele

50 , a member of the IL-5 family, also augments fMLP-stimulated ERK1/2 phosphorylation in primary eosino

51 rgistic activation of NF-kappaB by bacterial fMLP and TNFalpha may be involved in the induction of Re

52 important mechanism through which bacterial fMLP not only attracts leukocytes but also directly cont

53 Because fMLP-stimulated neutrophils produce leukotriene (LT)B4,

54 egrins in promoting close apposition between fMLP-stimulated PMN and fibrin containing surfaces, ther

55 These compounds also blocked fMLP-dependent chemotaxis in HL60 cells and primary huma

56 m Clostridium botulinum, effectively blocked fMLP-induced NF-kappaB activation as well as interleukin

57 eatum ssp. polymorphum significantly blocked fMLP-induced superoxide generation (P <0.001).

58 m and ssp. polymorphum significantly blocked fMLP-induced superoxide generation (P <0.001).

59 down of PRG, a GEF-deleted PRG mutant blocks fMLP-dependent RhoA activation and causes neutrophils to

60 Both fMLP-induced AA release and leukotriene C(4) (LTC(4)) se

61 Chemotaxis to both fMLP and WKYMVm was significantly reduced in isolated Ak

62 tivity, in contrast to oxidase activation by fMLP, where 70% of the response is eliminated by p38 MAP

63 rylation of gIV-PLA(2) at Ser(505) caused by fMLP, thus inhibiting gIV-PLA(2) hydrolysis and producti

64 on AA release or LTC(4) secretion caused by fMLP.

65 y [(32)P]orthophosphate loading, followed by fMLP stimulation in the presence and absence of a p38 MA

66 elial cells inhibit superoxide generation by fMLP and ANCA-activated neutrophils.

67 -induced chemotaxis, but not that induced by fMLP.

68 C prevented lung vascular injury mediated by fMLP-activated neutrophils.

69 sphate, and lysophosphatidic acid but not by fMLP or thapsigargin, whereas 13'-carboxychromanol decre

70 2-Chlorohexadecanal was also produced by fMLP-treated neutrophils.

71 Activation of Rac1 and Rac2 by fMLP was diminished in RhoG(-/-) neutrophils only at ver

72 stimulation for 24 hours with anti-IgE, C5a, fMLP, and IL-3 in basophils and by IL-3, IL-5, and IL-33

73 activation in response to a chemoattractant fMLP in mouse neutrophils.

74 filters toward the bacterial chemoattractant fMLP was more significantly inhibited by MALP-2 (TLR2/6

75 trophils stimulated with the chemoattractant fMLP were found to exhibit intense phosphorylation of a

76 lammatory G protein-coupled chemoattractants fMLP, platelet-activating factor, and IL-8 elicit unique

77 both to C5a and to the bacterial chemotaxin, fMLP.

78 e neutrophils in Zigmond chambers containing fMLP gradients.

79 when a physiological stimulus such as GM-CSF/fMLP is employed in the presence of thimerosal suggests

80 erosal in neutrophils stimulated with GM-CSF/fMLP was similar but more sustained compared with sample

81 n the effects of this compound on the GM-CSF/fMLP-stimulated neutrophil.

82 onse in basophils stimulated by the distinct fMLP receptor pathway.

83 oves to the granules and lipid bodies during fMLP-mediated activation.

84 not decline, and DNA was not cleaved during fMLP stimulation.

85 le in enhanced phospholipid movements during fMLP stimulation.

86 mponent downstream of the GTPase RhoA during fMLP-induced activation of NF-kappaB.

87 s, HL-60 clone-15 recapitulated the enhanced fMLP-induced ERK1/2 phosphorylation observed in primary

88 on stimulated by platelet-activating factor, fMLP, and SP-G.

89 family cytokines or the chemotactic factors fMLP, CCL5, and CCL11.

90 and suggests that in the presence of fibrin fMLP promotes bacterial virulence.

91 esponsible for Cbl phosphorylation following fMLP.

92 e identified several critical components for fMLP-induced NADPH oxidase activation.

93 near the constant of dissociation (K(d)) for fMLP binding to its receptor ( approximately 10 nM) craw

94 ession of the G protein-coupled receptor for fMLP did not affect chemotherapeutic agent-induced cytok

95 an neutrophils, AR activity was required for fMLP-included CD11b activation and up-regulation, respir

96 GTPase RhoA is a novel signal transducer for fMLP-induced NF-kappaB activation and Galpha(i) or Galph

97 ation by formylmethionylleucylphenylalanine (fMLP).

98 tractant formylmethionylleucylphenylalanine (fMLP).

99 ion with formylmethionylleucylphenylalanine (fMLP).

100 vated) of preactivated cells moved away from fMLP.

101 ted with activated gamma- and alpha-Pak from fMLP-stimulated neutrophils that contain the sequence KR

102 Furthermore, fMLP induces signal transduction including intracellular

103 ed with a variety of chemoattractants (e.g., fMLP).

104 r response to other activating agents, e.g., fMLP.

105 BL cells) expressing the high affinity human fMLP receptor FPR, but not parental RBL cells or cells t

106 as reported by Niggli, and also (ii) impairs fMLP-dependent frontness: pseudopods are flatter, contai

107 es monophosphorylated myosin light chains in fMLP-stimulated cells, and myosin II ATPase inhibition r

108 nted actin reorganization and the changes in fMLP-stimulated exocytosis induced by Hsp27 sequestratio

109 radients expose each cell to a difference in fMLP concentration (DeltaC) across its diameter that is

110 y that LPC inhibits superoxide generation in fMLP- and PMA-stimulated neutrophils without affecting f

111 (-/-) neutrophil recruitment was impaired in fMLP-induced transmigration into the cremaster muscle, t

112 ock activation of the 63- and 69-kDa Paks in fMLP-stimulated neutrophils.

113 ydrolysis of membrane phosphatidylcholine in fMLP-stimulated human blood eosinophils.

114 hese data supported a role for human PLD1 in fMLP-induced p38 activation in neutrophil-like HL-60 cel

115 es with p67(phox) and Rac2, but not Rac1, in fMLP-stimulated human neutrophils, correlating with supe

116 psilon, associates functionally with RhoA in fMLP-stimulated monocytes and that PKCepsilon acted as a

117 pecific anti-FcepsilonRI and IgE-independent fMLP stimulation was determined by basophil activation t

118 anol but not 2-butanol (0.05-0.5%) inhibited fMLP-induced p38 activation but did not inhibit p44/p42

119 i-Hsp27 Ab, but not an isotype Ab, inhibited fMLP-stimulated chemotaxis, increased cortical F-actin i

120 Inhibition of Akt activity also inhibited fMLP-stimulated neutrophil chemotaxis.

121 negative form of RhoA (T19N) also inhibited fMLP-stimulated reporter gene expression in a kappaB-dep

122 e absence of fMLP stimulation, and inhibited fMLP-stimulated exocytosis.

123 eltap85) concentration dependently inhibited fMLP-stimulated phosphorylation of protein kinase B, a d

124 ents or formylmethionyl-leucylphenylalanine (fMLP) induced a stiffening response within 2 minutes tha

125 i-IgE, formyl-methionyl-leucylphenylalanine (fMLP), or the Ca(2+) ionophore, A23187.

126 Like fMLP, dGal-1 rapidly elevated cytosolic Ca(2+) levels in

127 e naive unprimed PMN in suspension, 10(-5) M fMLP did, presumably via the low-affinity receptor, usin

128 .4, for 10(-9) M fMLP, and 7.3, for 10(-6) M fMLP, over nonstimulated cell values, determined to be 3

129 vided that [Ca(2+)](i) is restored, 10(-7) M fMLP, previously shown to elicit maximal Delta[Ca(2+)](i

130 fMLP but was not decreased with 1 x 10(-7) M fMLP, suggesting that neutrophils are specifically adapt

131 While exposure to 10(-7) M fMLP, which saturates the PMN high-affinity receptor, di

132 IL-8 mRNA increased 8-fold with 5 x 10(-9) M fMLP but was not decreased with 1 x 10(-7) M fMLP, sugge

133 lus increase by factors of 3.4, for 10(-9) M fMLP, and 7.3, for 10(-6) M fMLP, over nonstimulated cel

134 hibited polarized morphology of neutrophils, fMLP-stimulated PIP3 production and chemotaxis.

135 d 2A protein phosphatases) but not in normal fMLP-stimulated cells.

136 The basophil response to anti-IgE, but not fMLP or A23187, varied significantly across the 24 hours

137 xidase was confirmed based on the ability of fMLP to induce PKCdelta translocation and the sensitivit

138 The ability of fMLP to synergize with TNFalpha and activate NF-kappaB r

139 increased cortical F-actin in the absence of fMLP stimulation, and inhibited fMLP-stimulated exocytos

140 plete loss in binding of C5a, but binding of fMLP remained normal.

141 a hierarchy among these chemoattractants of fMLP > CXCL8 > CXCL2 > leukotriene B(4).

142 g surfaces, thereby inhibiting chemotaxis of fMLP-stimulated PMN through fibrin gels.

143 after exposure to a uniform concentration of fMLP.

144 were stimulated by uniform concentrations of fMLP and was enhanced further, to 99.4%, in the presence

145 in response to low vs high concentrations of fMLP.

146 elta[Ca(2+)](i) to a subsequent high dose of fMLP or IC; conversely, cells first exposed to 120 mug/m

147 We compared the effect of fMLP with those of tumor necrosis factor alpha (TNF alph

148 tivating agent and potentiates the effect of fMLP, 2) exogenous galectin-3 augments neutrophil phagoc

149 s NF-kappaB activation, and this function of fMLP requires phosphatidylinositol 3-kinase (PI3K).

150 s NF-kappaB activation, and this function of fMLP requires small GTPase RhoA in human peripheral bloo

151 se to a combination of a defined gradient of fMLP and an evolving gradient of LTB4, generated by cell

152 ophils inhibited the synergistic increase of fMLP-induced activation of Ras, ERK1/2 and Akt, as well

153 togen-activated protein kinase and a loss of fMLP-induced extracellular signal-related kinase phospho

154 in shedding after stimulation with 0.5 nM of fMLP.

155 ced binding to Por1, shows reduced rescue of fMLP-induced chemotaxis.

156 KCdelta translocation and the sensitivity of fMLP-induced O()(2) production to rottlerin, a PKCdelta-

157 to maximally mobilize PS to the surfaces of fMLP-activated neutrophils.

158 0, respectively, had only a modest effect on fMLP-elicited superoxide production and no effect on the

159 well as PAF-R agonists, yet had no effect on fMLP-mediated PAF-R agonist production.

160 d ETx exhibit distinct inhibitory effects on fMLP (and C5a) receptor-mediated superoxide production,

161 Also, in the in vitro experiments on fMLP-stimulated neutrophils and 5-LOX-transfected human

162 d the synergistic effects of IL-3 priming on fMLP-induced ERK1/2 phosphorylation.

163 ced imbalance between the divergent, opposed fMLP-induced "backness" and "frontness" signals responsi

164 IL-5, eotaxin-1, or fMLP caused 1) change of Mac-1 to its active conformatio

165 l cell-derived factor 1alpha (SDF-1alpha) or fMLP.

166 basophils following either anti-IgE, IL-3 or fMLP stimulation.

167 Tenascin did not affect leukotriene B4- or fMLP-stimulated expression of beta1 or beta2 integrins,

168 of oxidant generation in response to C5a or fMLP, but normal responses to PMA or opsonized zymosan a

169 lone or in combination with either GM-CSF or fMLP.

170 upled agonists platelet-activating factor or fMLP, but abolished agonist-stimulated Ca(2+) entry.

171 ANCA IgG or fMLP induced superoxide release when perfused over neutr

172 in Zigmond chambers containing IL-8, KC, or fMLP gradients.

173 after the cells were stimulated with LTB4 or fMLP.

174 rminal kinase, and Akt was induced by PMA or fMLP, which was decreased in rac2(-/-) neutrophils for E

175 degranulation, had no effect on TNFalpha- or fMLP-stimulated (3)H-DG uptake.

176 eptors for the bacterial chemotactic peptide fMLP are implicated in inflammation and host defense aga

177 ood neutrophils with the chemotactic peptide fMLP or with leukotriene B(4) or fibrinogen results in l

178 enuated by the bacterial chemotactic peptide fMLP, suggesting these two chemoattractants might share

179 TL and SKF inhibited chemotactic peptide fMLP-induced response linked to TRPV2 Ca(2+) activity, a

180 ial outer membrane, and formylated peptides (fMLP), a bacterial-derived peptide, induced proinflammat

181 ension stimulated with N-formyl-Met-Leu-Phe (fMLP was mostly dependent on PI3K, while the rate of int

182 emotactic responses to N-formyl-Met-Leu-Phe (fMLP) and interleukin-8 (IL-8/CXCL8) were studied using

183 otactic migration toward formyl-Met-Leu-Phe (fMLP) and stromal cell-derived factor 1alpha (SDF-1alpha

184 towards chemoattractant formyl Met-Leu-Phe (fMLP) coupled with their decreased polarization, and (iv

185 chemotactic peptide formylated Met-Leu-Phe (fMLP) demonstrated transient PS exposure.

186 e to the chemoattractant formyl-Met-Leu-Phe (fMLP) in adherent cells.

187 Chemoattractants like f-Met-Leu-Phe (fMLP) induce neutrophils to polarize by triggering diver

188 Chemoattractants such as formyl-Met-Leu-Phe (fMLP) induce neutrophils to polarize by triggering diver

189 Chemoattractants like fMet-Leu-Phe (fMLP) induce neutrophils to polarize with phosphatidylin

190 timulation with IL-8 and formyl-Met-Leu-Phe (fMLP) induced an increase in Cdc42 and Rac activation.

191 e previously demonstrated that fMet-Leu-Phe (fMLP) stimulates NF-kappaB activation, and this function

192 arized in response to uniform f-Met-Leu-Phe (fMLP), 42 polarized to the left of this arrow, 6 polariz

193 e that the formylated peptide f-Met-Leu-Phe (fMLP), a bacterial chemoattractant, synergizes with TNFa

194 ils upon activation with formyl-Met-Leu-Phe (fMLP), adenosine diphosphate (ADP), platelet-activating

195 g the bacterial peptide, formyl-Met-Leu-Phe (fMLP), as an RB inducer.

196 rted that the chemoattractant, fMet-Leu-Phe (fMLP), induces the activation of NF-kappaB in human peri

197 to glycoconjugates on N-formyl-Met-Leu-Phe (fMLP)-activated neutrophils exposes PS and facilitates n

198 nd the chemoattractant N-formyl-Met-Leu-Phe (fMLP)-coated beads.

199 d by the chemoattractant formyl-Met-Leu-Phe (fMLP).

200 oint source of an attractant, f-Met-Leu-Phe (fMLP).

201 to the bacterial peptide formyl-Met-Leu-Phe (fMLP).

202 emoattractants such as N-formyl-Met-Leu-Phe (fMLP).

203 ients of the chemoattractant, f-Met-Leu-Phe (fMLP).

204 ); Interleukin-8 (IL-8); formyl-Met-Leu-Phe (fMLP); monocyte chemotactic protein 1 (MCP1).

205 derived chemoattractant (formyl-met-leu-phe, fMLP), with and without preactivation by interleukins (i

206 formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP) (1 muM) stimulation.

207 Formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP) and after pretreatment of the cells with cocoa pol

208 formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP)-stimulation on its mechanical properties (elastic

209 ant formyl-methionine-leucine-phenylalanine (fMLP).

210 ses to formylmethionyl-leucyl-phenylalanine (fMLP) and IL-8 were dose-dependently inhibited by treatm

211 ds to formyl-methionyl-leucyl-phenylalanine (fMLP) and plays a role in neutrophil chemotaxis, has bee

212 to N-formyl-methionyl-leucyl-phenylalanine (fMLP) and/or multivalent immune complexes (IC).

213 ant N--formylmethionyl-leucyl-phenylalanine (fMLP) is mediated by leukotriene B4 (LTB4).

214 ith N-formyl-methionyl-leucyl-phenylalanine (fMLP) results in biphasic activation of PI3K; the first

215 ctant formyl-methionyl-leucyl-phenylalanine (fMLP) stimulated p38-MAPK-dependent phosphorylation of 1

216 with formyl-methionyl-leucyl-phenylalanine (fMLP) stimulates cells in a physiologically relevant man

217 to N-formyl-methionyl-leucyl-phenylalanine (fMLP) stimulation.

218 out N-formylmethionine leucyl-phenylalanine (fMLP) stimulation.

219 muM N-formyl-methionyl-leucyl-phenylalanine (fMLP) triggered earlier and more sustained O(2)(-) gener

220 de (N-formyl-methionyl-leucyl-phenylalanine (fMLP)), platelet activating factor (PAF), leukotriene B4

221 of N-formyl-methionyl-leucyl-phenylalanine (fMLP), as occurs in hPepT1 expressing Caco2-BBE cells.

222 ed to formyl-methionyl-leucyl-phenylalanine (fMLP), PKCbetaII was rapidly phosphorylated and physical

223 the N-formyl-methionyl-leucyl-phenylalanine (fMLP)-induced neutrophil respiratory burst.

224 of N-formyl-methionyl-leucyl-phenylalanine (fMLP)-mediated formation of CysLT.

225 s of N-formylmethionyl-leucyl-phenylalanine (fMLP)-mediated neutrophil migration was significantly di

226 that formyl-methionyl-leucyl-phenylalanine (fMLP)-stimulated respiratory burst activity and (3)H-DG

227 Combined stimulation with EMD plus fMLP resulted in significantly higher chemotaxis compare

228 xogenous expression of p40(phox) potentiated fMLP-induced O()(2) production and raised the level of O

229 Also, ethanol prevented fMLP-induced CD11b up-regulation.

230 bitors of PIP3 synthesis completely prevents fMLP from activating a PIP3-dependent kinase and Cdc42 b

231 , formyl peptide receptor (FPR), the primary fMLP receptor, partitioned to high density fractions, co

232 antly less O(2)( ) in response to LPS-primed fMLP and translocated less p67(phox) than normal PMN, al

233 ide first direct evidence for reconstituting fMLP-induced O()(2) production in a nonhemopoietic cell

234 Neutrophils from Rap1a-/- mice had reduced fMLP-stimulated superoxide production as well as a weake

235 In addition, LPC reduced fMLP-stimulated phosphorylation of ERK and Akt and membr

236 PIP3-deficient cells show reduced fMLP-dependent Rac activity and unstable pseudopods, whi

237 FACS analysis with and without stimulation (fMLP 5 micromol/L or PMA 5 micromol/L).

238 romoenol lactone (BEL) completely suppressed fMLP-induced generation of superoxide.

239 ll-molecule Gbetagamma inhibitors suppressed fMLP-stimulated Rac activation, superoxide production, a

240 Furthermore, SLURP1 suppressed fMLP-induced phosphorylation of protein kinase-B (AKT) i

241 N bacterial killing in fibrin gels, and that fMLP inhibits PMN bactericidal activity in fibrin gels.

242 fecting respiratory burst activity, and that fMLP stimulation of TNFalpha-primed cells causes major u

243 t evidence that fMLP activates RhoA and that fMLP-induced NF-kappaB activation requires this small GT

244 Here we present evidence that fMLP activates RhoA and that fMLP-induced NF-kappaB acti

245 ermit dGal-1 to mobilize PS, indicating that fMLP initiated both Ca(2+)-dependent and -independent si

246 We reported previously that fMLP stimulates NF-kappaB activation, and this function

247 lation of intracellular Ca(2+) revealed that fMLP and dGal-1 independently release Ca(2+) from intrac

248 ndings demonstrate, for the first time, that fMLP-induced activation of NF-kappaB utilizes a signalin

249 The fMLP-induced adhesion and motility of fibroblasts on fib

250 However, rapamycin did not alter the fMLP-induced membrane association of p47phox and p38-MAP

251 l kinase, and cPLA2alpha also attenuated the fMLP-mediated formation of CysLT.

252 Selective sPLA2-X inhibition attenuated the fMLP-mediated release of arachidonic acid and CysLT form

253 In contrast, the fMLP-stimulated change in neutrophil shape was not influ

254 of untreated neutrophils moved away from the fMLP signal, while only 15.2 or 22.2% (interleukin-2-or

255 However, the fMLP-stimulated neutrophils exhibited a significant decr

256 ell polarization and the augmentation of the fMLP-induced superoxide anion generation, by all priming

257 asma containing HNA-3a antibodies primed the fMLP-activated respiratory burst of HNA-3a+, but not HNA

258 cells were still capable of prioritizing the fMLP signal over a competing chemoattractant, leukotrien

259 viated from the expected movement toward the fMLP signal.

260 s of spontaneous migration and chemotaxis to fMLP and IL-8.

261 we demonstrate that neutrophil chemotaxis to fMLP is dependent on Ca++ mobilization mediated by cycli

262 significantly higher chemotaxis compared to fMLP alone (P <0.05).

263 The mTOR contribution to fMLP-induced RB, phosphorylation of p47phox and p38-MAPK

264 with the defect in chemotactic migration to fMLP.

265 is, respond chemokinetically, in reaction to fMLP.

266 cessary for the COS-phox cells to respond to fMLP.

267 and the formyl peptide receptor responded to fMLP with a approximately 7- to 10-fold increase in luci

268 he subsequent oxidative burst in response to fMLP as assessed by oxidation of dihydrorhodamine 123 (d

269 otriene C(4) release observed in response to fMLP in "primed" eosinophils.

270 MMP-8 secretion by PMNs in response to fMLP or serum-opsonized zymosan stimulation was signific

271 he response to A23187, while the response to fMLP was significantly higher at 08:00 vs. 20:00 in cont

272 activation and ROS production in response to fMLP, these responses are substantially lower and largel

273 t of LTB4, generated by cells in response to fMLP.

274 oated SRBC, and almost absent in response to fMLP.

275 owed enhanced p84-dependent ROS responses to fMLP and C5a, suggesting that competition may exist betw

276 ts with stage I COPD had normal responses to fMLP and IL-8, subjects with more severe stage II-IV COP

277 ad no effect on either of these responses to fMLP.

278 utant significantly reduced migration toward fMLP, whereas none of the Hsp27 proteins affected fMLP-s

279 , and that recruitment of neutrophils toward fMLP in vivo is reduced in these mice.

280 The migration of neutrophils toward fMLP was similarly not affected by the syk(-/-) mutation

281 Unlike fMLP, CaG did not induce potent Ca(2+) flux and was a re

282 In vivo, fMLP induced neutropenia, sequestration of neutrophils w

283 otentially important mechanism through which fMLP not only attracts leukocytes but may also contribut

284 ribution of PS on neutrophils activated with fMLP and dGal-1.

285 Neutrophils were activated with fMLP, normal IgG, or ANCA IgG.

286 phil elastase secretion upon activation with fMLP, ADP, PAF, IL-8, C5a, and LTB(4) was normal, as wer

287 cal increase in (3)H-DG uptake compared with fMLP without affecting respiratory burst activity, and t

288 Stimulation of monocytes with fMLP rapidly activated RhoA as well as NF-kappaB, and th

289 Stimulation of monocytes with fMLP resulted in activation of both PKCepsilon and NF-ka

290 Activation of neutrophils with fMLP up-regulated the ligand-binding function of CD32A,

291 Activation of neutrophils with fMLP, however, did not significantly alter surface label

292 cells were stimulated with IL-8 but not with fMLP.

293 Stimulation of PMN with fMLP resulted in increased surface expression of these S

294 n peripheral blood monocytes stimulated with fMLP and that Lbc specifically catalyzes the guanine nuc

295 Neutrophils stimulated with fMLP or a variety of other chemoattractants that bind to

296 ults suggested that in cells stimulated with fMLP, PLD was upstream of p38.

297 and Thr(402) in neutrophils stimulated with fMLP.

298 n fibroblasts and find that stimulation with fMLP triggers dose-dependent migration of these cells.

299 During stimulation with fMLP, a chemotactic factor, two Ca2+ waves traveling in

300 er mother when neutrophils were treated with fMLP with or without platelet-activating factor, PMA alo