ライフサイエンスコーパス: LTB4

1 ral neutrophil chemotaxis is leukotriene B4 (LTB4).

2 a competing chemoattractant, leukotriene B4 (LTB4).

3 he chemotactic gradient with leukotriene B4 (LTB4).

4 lanine (fMLP) is mediated by leukotriene B4 (LTB4).

5 tion of a second eicosanoid, leukotriene B4 (LTB4).

6 e site, probably preventing tight docking of LTB4.

7 he formation of the proinflammatory mediator LTB4.

8 zation with the neutrophil chemotactic agent LTB4.

9 red engagement of receptors for both MIF and LTB4.

10 d BLT2 mRNA and inhibited their migration to LTB4.

11 f their expression of BLT1, the receptor for LTB4.

12 before intraluminal injection of toxin A or LTB4.

13 tandem mass spectrometry for metabolites of LTB4.

14 tadecatrienoic acid, LTB4, and 10,11-dihydro-LTB4.

15 phil adhesion and degranulation responses to LTB4.

16 insulin sensitization, possibly by reducing LTB4.

17 ized including 17-, 18-, 19-, and 20-hydroxy-LTB4, 10-hydroxy-4,6,12-octadecatrienoic acid, LTB4, and

18 ucuronide (16.7-29.4 pmol/ml) and 20-carboxy-LTB4 (18.9-30.6 pmol/ml) present in the urine of subject

19 ibitor effectively reduced the production of LTB4 (23.7% decrease) and significantly reduced TNF and

20 inhibitor effectively reduced production of LTB4 (23.7% decrease) and significantly reduced TNF and

21 vs 2.41 pg/mL EBC, respectively [P < .001]; LTB4: 45.62 vs 3.82 pg/mL EBC, respectively [P < .001]).

22 rat (SHR) support a role for leukotriene B4 (LTB4 ), a potent chemoattractant involved in the inflamm

23 rat (SHR) support a role for leukotriene B4 (LTB4 ), a potent chemoattractant involved in the inflamm

24 They are the main source of leukotriene B4 (LTB4), a potent proinflammatory lipid mediator.

25 Leukotriene B4 (LTB4), a proinflammatory mediator produced by the enzyme

26 ghly unstable epoxide intermediate LTA4 into LTB4, a potent leukocyte activating agent, while the ami

27 LTB4, a product of the innate immune response, is a cons

28 al mechanisms mediated by neutrophil-derived LTB4 act through activation of its receptor, B leukotrie

29 Leukotriene B4 (LTB4) activates the G-protein-coupled receptor leukotrie

30 findings establish that the exosomal pool of LTB4 acts in an autocrine fashion to sensitize neutrophi

31 LTB4 also stimulated TRPV1-mediated substance P release

32 1 selectively blocks conversion of LTA4 into LTB4, although sparing the enzyme's anti-inflammatory am

33 nd bone resorption in vitro, suggesting that LTB4 and BLT1 could be effectively targeted for the trea

34 Co-application of LTB4 and cholane steroid did not further increase LTB4-i

35 cytes from subjects with AERD generated more LTB4 and cysteinyl LTs than did granulocytes from contro

36 ar exclusion of 5-LOX and thereby suppresses LTB4 and enhances LXA4 in macrophages.

37 ransgenic mice that included lower levels of LTB4 and increased amounts of lipoxin A4 compared with n

38 ed the developed method to the separation of LTB4 and its coeluting isomer 5S,12S-diHETE in murine pe

39 l of neutrophil signal relay that focuses on LTB4 and its exosome-mediated secretion.

40 Our data show that LTB4 and its receptor BLT1 exacerbate synovial inflammat

41 In this study we investigated the role of LTB4 and its receptor LTB4R1 (BLT1) in synovial inflamma

42 Here, we show that LTB4 and its synthesizing enzymes localize to intracellu

43 ontributing to the synthesis of leukotrienes LTB4 and LTC4, mediators of inflammation and pain, were

44 T2-R protein expression and higher levels of LTB4 and LTC4/D4/E4 emerged in children with obstructive

45 s LT1-R and LT2-R, and for concentrations of LTB4 and LTC4/D4/E4.

46 ese results suggest that the balance between LTB4 and PGE2 determines the amount of IL-1beta inflamma

47 4 and PGE2, whereas the relationship between LTB4 and PGE2 was not as strong.

48 s were associated with a gradual decrease of LTB4 and PGE2, and a gradual increase in CXCL1 and CCL2.

49 ritis in mice and showed that elevated serum LTB4 and synovial expression of 5-lipoxygenase correlate

50 We demonstrate that AAT can bind LTB4 and that AAT/LTB4 complex formation modulates BLT1

51 ion of neutrophils induces the production of LTB4 and TNF by infected macrophages, leading to the con

52 granulation reverted this effect, abolishing LTB4 and TNF production.

53 in vitro was sufficient to suppress release LTB4 and to protect epithelial cells in co-culture.

54 dance of the proinflammatory leukotriene B4 (LTB4) and a corresponding decrease in the level of prore

55 or other chemotaxins such as leukotriene B4 (LTB4) and fMLP is unknown.

56 naling through the chemokine leukotriene B4 (LTB4) and its receptor LTB4R1.

57 Eicosanoids, such as leukotriene B4 (LTB4) and lipoxin A4 (LXA4), may play a key role during

58 of interleukin 8 (IL-8) and leukotriene B4 (LTB4) and was prevented by mitochondrial antioxidant.

59 n inhibitory factor (MIF), leukotriene B(4) (LTB4), and high mobility group box 1 protein (HMGB1) and

60 B4, 10-hydroxy-4,6,12-octadecatrienoic acid, LTB4, and 10,11-dihydro-LTB4.

61 Enzyme immunoassay determined LTB4, and enzyme-linked immunosorbent assays quantified

62 L. amazonensis in the presence of exogenous LTB4, and macrophages obtained from P2X7 receptor knocko

63 the urine from those subjects injected with LTB4, and none were present in the urine from the placeb

64 han CysLT1, the role of another class of LT, LTB4, and the potential role of LTs in lung diseases oth

65 demonstrated that lipophilic (99m)Tc-labeled LTB4 antagonist 1 (RP517) accumulated in infectious foci

66 Divalent LTB4 antagonist 17 (DPC11870-11) is a DTPA conjugate for

67 B4 antagonists 15 (BMS57868-88) and divalent LTB4 antagonist 18 (BMS57868-81) are conjugated to bifun

68 Monovalent LTB4 antagonists 15 (BMS57868-88) and divalent LTB4 anta

69 The biodistribution of the (99m)Tc-labeled LTB4 antagonists was affected by the coligands used with

70 Exogenous administration confirms LTB4 anti-inflammatory activity and abrogates TsV-induce

71 ally thought to be pathogenic, low levels of LTB4 are actually beneficial in maintaining tendon tissu

72 The actions of LTB4 are mediated by two cell surface receptors, BLT1, w

73 prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) are implicated in the development of tendinopathy.

74 thesis of the lipid mediator leukotriene B4 (LTB4) are pivotal components of host defense and inflamm

75 ipoxygenase and its product, leukotriene B4 (LTB4), are highly expressed in several human pathologies

76 of SPMs to pro-inflammatory leukotriene B4 (LTB4), are significantly decreased in the vulnerable reg

77 odel enables us to determine the gradient of LTB4 arising either through directed secretion from cell

78 Moreover, the identification of LTB4 as a highly potent ligand for BK channels is critic

79 se data provide new evidence for the role of LTB4 as an important neuro-immune pathway in the develop

80 sulted in the formation of PGE2, 5-HETE, and LTB4 as the principal metabolites of COX-2 and 5-LOX, re

81 cell proliferation compared to controls and LTB4 at 0.1 nM negated the PGE2-induced decrease in cell

82 ignificantly diminished by co-treatment with LTB4 at 0.1 nM.

83 The results showed that LTB4 at low doses (0.1 and 1 nM) significantly increased

84 LTB4, at low concentrations, promoted the migration of i

85 , we evaluated the participation of the 5-LO/LTB4 axis in graft-versus-host disease (GVHD) pathogenes

86 Our data provide evidence that the 5-LO/LTB4 axis orchestrates GVHD development and suggest it c

87 A2/5-lipoxygenase/leukotriene-B4 (PLA2/5-LOX/LTB4) axis is an important inflammatory signaling pathwa

88 We show that the C5 and LTB4 binding activities of the molecule are independent

89 equally dependent on both C5 inhibition and LTB4 binding for full activity.

90 Here, we examined the effect of LTB4 binding on OmCI structure and function and investig

91 of these metabolites could be used to assess LTB4 biosynthesis following activation of the 5-lipoxyge

92 Inhibition of the LTB4 biosynthetic enzyme 5-lipoxygenase inhibited toxin

93 ate that a neutrophil-T cell axis reliant on LTB4-BLT1 interaction is required for allergic skin infl

94 A role for the LTB4-BLT1 pathway in allergen-induced airway hyperrespon

95 To directly assess the role of the LTB4-BLT1 pathway in atherogenesis, we bred BLT1(-/-) mi

96 ne the important role for mast cells and the LTB4-BLT1 pathway in the development of CD8+ T cell-medi

97 Activation of LTB4-BLT1/2 pathway decreases cAMP generation, controlli

98 These results suggest that the LTB4/BLT1 axis sets the pace of CS-induced sterile infla

99 on and ERK1/2 phosphorylation in response to LTB4 but had no effect on either of these responses to f

100 imately 0.5 muM) and conversion of LTA4 into LTB4 by purified LTA4H with a Ki of 2.3 muM.

101 pendent on the generation of leukotriene B4 (LTB4) by neutrophils and their expression of the LTB4 re

102 nding a C16 fatty acid and the other binding LTB4 (C20).

103 r ICAM-2 rapidly released TNF in response to LTB4, C5a, and KC.

104 generation and its relationship to PGE2 and LTB4 can be visualized as an important marker for the pa

105 Blocking the 5LO/LTB4 cascade inhibited viral latent ORF73, immunomodulat

106 neuroinflammation via activating PLA2/5-LOX/LTB4 cascade using a partial frontal lobe resection SBI

107 outcomes after SBI by activating PLA2/5-LOX/LTB4 cascade.

108 LTB4 caused ileitis similar to that caused by toxin A an

109 onstrate that AAT can bind LTB4 and that AAT/LTB4 complex formation modulates BLT1 engagement and dow

110 th AAT augmentation therapy decreased plasma LTB4 concentrations and reduced levels of membrane-bound

111 A4 concentrations negatively correlated with LTB4 concentrations and with exacerbation numbers in chi

112 We examined LXA4 and LTB4 concentrations in induced sputum supernatants from

113 ontrast to decreases in LXA4 concentrations, LTB4 concentrations were increased in children with asth

114 Leukotriene B4 (LTB4) contributes to many inflammatory diseases, includi

115 study, we investigated the possibility that LTB4 control of MyD88 expression involves the generation

116 In particular, neutrophil-derived LTB4 controls L. amazonensis killing, degranulation, and

117 Migration to LTB4 could be inhibited by either a BLT1- or BLT2-select

118 These results suggest that low levels of LTB4 counterbalance the negative effects mediated by PGE

119 An LTB4 cutoff value of 11 pg/mL EBC provides 100% sensitiv

120 nge, LTD4 and LTE4 increased, while PGE2 and LTB4 decreased in AERD subjects only.

121 Furthermore, LTB4 decreased insulin receptor tyrosine phosphorylation

122 Recently, BLT1 expression and LTB4-dependent chemotaxis have been reported in immature

123 In vitro treatment with LTB4 directly enhanced macrophage chemotaxis, stimulated

124 Computational modeling predicted that LTB4 docked onto the cholane steroid-sensing site in the

125 eukotriene synthesis, our findings reveal an LTB4-driven autocrine/paracrine regulatory effect.

126 evels of 5LO and high levels of secretion of LTB4 during primary KSHV infection of endothelial cells

127 LTB4 elicited BLT1-dependent chemotaxis in effector cell

128 Our results demonstrate that LTs, especially LTB4, enhanceAM microbicidal activity through the PKC-de

129 -/-) mice, which have a functional defect in LTB4 expression, also failed to induce uveitis in the re

130 LTB4 failed to activate beta1 subunit-containing channel

131 es, and more specifically on leukotriene B4 (LTB4), for disease induction as well as perpetuation.

132 icate that P2X7 receptor activation leads to LTB4 formation, which is required for L. amazonensis eli

133 ic 13S,14S-epoxide inhibited leukotriene B4 (LTB4) formation by human leukotriene A4 hydrolase (LTA4H

134 Phase I Clinical Trial of human tolerance to LTB4, four human subjects were injected with 150 nmol/kg

135 Recent evidence suggests that the release of LTB4 from cells occurs through packaging in exosomes.

136 gradient of fMLP and an evolving gradient of LTB4, generated by cells in response to fMLP.

137 erent neutrophils correlated positively with LTB4 generation and inversely with responsiveness to PGE

138 The PKA inhibitor H89 potentiated LTB4 generation by control granulocytes but was inactive

139 required for migration to HXA3 signals, but LTB4 generation by migrated neutrophils plays a signific

140 Reduced LTB4 generation in mutants could not be attributed to di

141 eloped novel compounds that potently inhibit LTB4 generation whilst leaving PGP degradation unperturb

142 The amount of LTB4 glucuronide (16.7-29.4 pmol/ml) and 20-carboxy-LTB4

143 mechanism that regulates the development of LTB4 gradients.

144 the presence of CP105696, an antagonist for LTB4 high-affinity receptor, ATP was not able to reduce

145 The urinary metabolites of LTB4 identified in this investigation were excreted in l

146 f HK formation paralleled that of 5-HETE and LTB4, implying the availability of the 5S-HETE substrate

147 Both HMC-1 cells and mBMMCs migrated to LTB4 in a dose-dependent manner in chemotaxis assays.

148 e importance of C-mediated C5 activation and LTB4 in a mouse model of immune complex-induced acute lu

149 inyl leukotrienes produced at the expense of LTB4 in AERD subjects.

150 The data highlight the importance of LTB4 in IC-ALI and activation of C5 by the complement pa

151 eriments demonstrate a nonredundant role for LTB4 in inflammatory arthritis and define a neutrophil m

152 Here we evaluated the roles of Syk and LTB4 in macrophage phagocytosis of apoptotic thymocytes

153 However, the role of LTB4 in mediating innate immune responses elicited by sp

154 However, the role of LTB4 in neutrophil infection by Leishmania amazonensis i

155 higher levels of the chemotactic eicosanoid LTB4 in obese high-fat diet (HFD)-fed mice.

156 The results demonstrate a critical role for LTB4 in ocular inflammation and in the development and p

157 esults provide strong evidence for a role of LTB4 in regulating DC migration and the induction of ada

158 Furthermore, a role for endogenous LTB4 in Syk activation during FcgammaR-mediated phagocyt

159 ctly responsible for neutrophil synthesis of LTB4 in the context of Pseudomonas aeruginosa-induced ne

160 d its chemotactic metabolite leukotriene B4 (LTB4) in KSHV biology.

161 synthesis and production of leukotriene B4 (LTB4) in myeloid cells, which modulate inflammatory arth

162 ated the mechanistic role of leukotriene B4 (LTB4) in the molecular pathogenesis of lymphedema.

163 counterregulatory compound, leukotriene B4 (LTB4), in patients with childhood asthma.

164 We predict that the secondary release of LTB4 increases recruitment range and show that the exoso

165 -PI3K immunoprecipitates obtained 30 s after LTB4, indicating a physical interaction between PSDP and

166 ocation of p47phox to the cell membrane, and LTB4 induced phosphorylation of p47phox in a manner depe

167 Stimulation of mBMMCs with LTB4 induced transient, dose-dependent, ERK phosphorylat

168 activating factor (PAF)- and leukotriene B4 (LTB4)-induced responses.

169 and cholane steroid did not further increase LTB4-induced activation.

170 B4 with LTA4, LTC4, LTD4, or LTE4 suppressed LTB4-induced activation.

171 t disrupting lipid raft integrity suppresses LTB4-induced activation.

172 es in ileal LTB4 levels and toxin A- but not LTB4-induced ileitis.

173 1 receptors but not LTB4 receptors inhibited LTB4-induced inflammation.

174 ific substance P-receptor antagonist blocked LTB4-induced substance P action and ileitis.

175 t neutrophil elastase is a key player in the LTB4 inflammatory cycle in AATD, causing increased LTB4

176 harmacologic 5-LO inhibition by zileuton and LTB4 inhibition by CP-105,696.

177 5LO/LTB4 inhibition downregulated TH2-related cytokine secre

178 5LO/LTB4 inhibition reduced fatty acid synthase (FASN) promo

179 As LTB4 is an important proinflammatory product of macropha

180 Thus, our findings suggest that although LTB4 is generally thought to be pathogenic, low levels o

181 While LTB4 is involved in adipose tissue inflammation and insu

182 urine peritoneal exudate cells, showing that LTB4 is present only after zymosan A injection while its

183 d on these findings, we investigated whether LTB4 is produced upon P2X7 receptor activation and exami

184 ial-derived HXA3 signals, neutrophil-derived LTB4 is required to amplify the magnitude of neutrophil

185 Leukotriene B4 (LTB4) is a potent activator and chemoattractant for leuk

186 Leukotriene B4 (LTB4) is a potent chemoattractant for neutrophils and is

187 Leukotriene B4 (LTB4) is a rapidly synthesized, early leukocyte chemoatt

188 he pro-inflammatory mediator leukotriene B4 (LTB4) is implicated in the pathologies of an array of di

189 esponsiveness (AHR) and that leukotriene B4 (LTB4) is involved in the chemotaxis of effector CD8+ T c

190 Leukotriene B4 (LTB4) is secreted by chemotactic neutrophils, forming a

191 inhibited toxin A-induced increases in ileal LTB4 levels and toxin A- but not LTB4-induced ileitis.

192 EBC LXA4 and LTB4 levels are increased in asthmatic patients compared

193 FLAP inhibitor MK886 were required to reduce LTB4 levels in exudates of female versus male mice and r

194 Moreover, reduction of LTB4 levels in gingival tissues was associated with a si

195 Moreover, reduction of LTB4 levels in the gingival tissues was associated with

196 se tissue had higher LXA4 rather than higher LTB4 levels, were leaner, and showed increased energy ex

197 elationship based on ex vivo leukotriene B4 (LTB4) levels in dog.

198 asured lipoxin A4 (LXA4) and leukotriene B4 (LTB4) levels in EBC collected from patients with asthma

199 nhanced arginase 1 and lower leukotriene B4 (LTB4) levels were detected in macrophages stimulated wit

200 e observations elucidate a novel role of the LTB4-Ltb4r1 signaling pathway in hepatocyte and myocyte

201 esistance and suggest that inhibition of the LTB4/LTB4R1 axis might be a useful approach for developi

202 Leukotrienes (LTA4, LTB4, LTC4, LTD4, and LTE4) are inflammatory lipid media

203 nd leukotriene (LT)E4 , induced sputum fluid LTB4 , LTE4 , PGD2 , and PGE2 , plasma secretory phospho

204 's ability to decrease nuclear 5-LOX and the LTB4:LXA4 ratio in vitro and in vivo was mimicked by mac

205 dings suggest that dual inhibition of C5 and LTB4 may be useful for treatment of human immune complex

206 However, the mechanism for LTB4 -mediated inflammation in hypertension is poorly un

207 inst miR-155 and miR-146b prevented both the LTB4-mediated decrease in SOCS-1 and increase in MyD88.

208 LTB4-mediated miR-155 generation was attributable to act

209 LTB4 mediates the inflammatory effects of toxin A via ac

210 e tested the hypothesis that leukotriene B4 (LTB4) mediates the effects of toxin A via activation of

211 These findings indicate that the MIF and LTB4 mediator pathways are involved in the immunopathoge

212 R expression that, associated with increased LTB4, might be involved in a reduction in the ability of

213 2X7 receptor activation and examined whether LTB4 modulates parasite elimination.

214 The results identify local LTB4-NE axis as a promoter of neutrophil rTEM and provid

215 as not influenced by exogenous or endogenous LTB4 nor associated with Syk activation (phosphorylation

216 The chemotactic activity of LTB4 on naive and IRBP-specific autoreactive T cells as

217 tudy was to determine the effect of PGE2 and LTB4 on the proliferation of human patellar tendon fibro

218 eserved after the cells were stimulated with LTB4 or fMLP.

219 Sputum LTB4 (P = 0.013), and plasma 11betaPGF2alpha (P = 0.032)

220 cute pleurisy through the synthesis of PGE2, LTB4, PAF, and IL-1beta.

221 ogy and that effective inhibition of the 5LO/LTB4 pathway could potentially be used in treatment to c

222 To further investigate the effect of the LTB4 pathway in bone loss, we performed osteoclast diffe

223 nalyses revealed that combined assessment of LTB4, PGE2 and CXCL1 was able to distinguish dogs with d

224 these findings collectively suggest that 5LO/LTB4 play important roles in KSHV biology and that effec

225 0% reduction) in response to leukotriene B4 (LTB4) plus prostaglandin E2 (PGE2) as well as approximat

226 We have shown that leukotriene (LT) B4 (LTB4) positively regulates macrophage MyD88 expression b

227 Inflammasome activation triggers LTB4 production and further PGE2 via IL-1beta/IL-1R sign

228 duced neutrophil recruitment is dependent on LTB4 production by mast cells and BLT1 expression on neu

229 CS exposure induces LTB4 production by mast cells and macrophages independen

230 tment and accumulation of MCs in response to LTB4 production in areas of inflammation.

231 LT)B4, we examined the effect of propofol on LTB4 production in vivo and in vitro Cecal ligation and

232 nflammatory cycle in AATD, causing increased LTB4 production, and associated BLT1 membrane receptor e

233 , gene expression profiling data showed that LTB4 production, degradation and downstream signalling i

234 gene expression profiling data showing that LTB4 production, degradation and downstream signalling i

235 ationship and a dose-dependent inhibition of LTB4 production.

236 ce neutrophil activation, degranulation, and LTB4 production.

237 ated the functional role of these pockets in LTB4 production.

238 5-LO) activity and increased leukotriene B4 (LTB4) production have been implicated in various inflamm

239 4 (15-epi-LXA4), lipoxin A4, leukotriene B4 (LTB4), prostaglandin E2 (PGE2), and interleukin (IL)-6 a

240 re increased in asthmatic patients, the LXA4/LTB4 ratio decreases with increasing asthma severity.

241 during plaque progression restores the RvD1:LTB4 ratio to that of less advanced lesions and promotes

242 Chronic blockade of the LTB4 receptor 1 (BLT1) receptor with CP-105,696, reduced

243 When LTB4 receptor 1 (BLT1) receptors were blocked with CP-10

244 ice could be blocked by administration of an LTB4 receptor antagonist confirming the role of BLT1 in

245 ) by neutrophils and their expression of the LTB4 receptor BLT1.

246 e reduced in mice lacking either 5-LO or the LTB4 receptor BTL1, and that macrophages from these mice

247 1B and PTEN, these effects being mediated by LTB4 receptor BTL1.

248 Inhibition of the LTB4 receptor Ltb4r1, through either genetic or pharmaco

249 e B6 mice, suggesting that expression of the LTB4 receptor on both activated autoreactive T cells and

250 f MIF or blockade of the MIF receptor and/or LTB4 receptor resulted in protection from LPS-induced AL

251 leukotriene receptor-1 (BLT-1), the primary LTB4 receptor, partitioned to low density fractions, co-

252 rophils and elicit chemotactic activity in a LTB4 receptor-dependent manner.

253 ase or via antagonism of the leukotriene B4 (LTB4) receptor.

254 A and antagonism of TRPV1 receptors but not LTB4 receptors inhibited LTB4-induced inflammation.

255 study demonstrates expression of functional LTB4 receptors, both BLT1 and BLT2, in murine and human

256 (BM-DCs) express functional leukotriene B4 (LTB4) receptors as observed in dose-dependent chemotaxis

257 It has been reported that leukotriene B4 (LTB4) reduces the parasitic load of infected macrophages

258 duction events, with Syk activation being an LTB4-regulated event in FcgammaR-mediated but not apopto

259 In this study we assessed whether AATD is an LTB4-related disease and investigated the ability of ser

260 clinical applications in treatment of other LTB4-related diseases.

261 In addition, ATP was sufficient to induce LTB4 release from infected control macrophages but not f

262 irectional motility with concomitant loss of LTB4 release.

263 Homomeric cbv1 or cbv1-beta2 channels were LTB4-resistant.

264 Only LTB4 reversibly increased BK steady-state activity (EC50

265 nked to oxidative stress leading to IL-8 and LTB4 secretions.

266 We conclude that HXA3 and LTB4 serve independent roles to collectively coordinate

267 array analysis revealed a promoting role of LTB4, showing a significant increase of CCR7 and CCL19 m

268 stigated the ability of serum AAT to control LTB4 signaling in neutrophils.

269 by which AAT augmentation therapy impacts on LTB4 signaling in vivo, and not only reinforces the util

270 LTB4 signaling is not required for migration to HXA3 sig

271 Supplementation of CM-O with LTB4 suppressed insulin sensitization and increased PTP1

272 drolase (LTA4H) catalyses the distal step in LTB4 synthesis and hence inhibitors of this enzyme have

273 ophil transepithelial migration by mediating LTB4 synthesis during migration, which serves to amplify

274 soform has been specifically shown to direct LTB4 synthesis in certain contexts.

275 thiazol-2-amine, denoted ARM1, that inhibits LTB4 synthesis in human neutrophils (IC50 of approximate

276 ency (IC50 < 10 nM) and potent inhibition of LTB4 synthesis in human whole blood (IC50 < 100 nM).

277 Pharmacologic blockade of LTB4 synthesis inhibited allergic skin inflammation elic

278 ed in whole blood and found to down-regulate LTB4 synthesis, displaying 45% inhibition at 10 microM.

279 ed upstream event for L. amazonensis-induced LTB4 synthesis.

280 tioning plays in determining leukotriene B4 (LTB4) synthesis.

281 but not neutrophils deficient in BLT1 or the LTB4-synthesizing enzyme LTA4H, restored the ability of

282 re similar to PGE2, but less than 5-HETE and LTB4 The time course of HK formation paralleled that of

283 y, and decreased levels of serum and hepatic LTB4 These results were associated with inhibition of le

284 Finally, neither PGE2 nor LTB4 treatment affected collagen type I gene expression.

285 LTB4 triggered SMC chemotaxis, which was pertussis toxin

286 In human neutrophils, leukotriene B4 (LTB4) triggered rapid decreases in PSDP and reciprocal i

287 ene (LT)E4, 9alpha, 11beta-prostaglandin F2, LTB4, tumor necrosis factor-alpha, and interleukin-1beta

288 Our data show that LTB4, via its receptor B leukotriene receptor 1 (BLT1) a

289 LTs increased H2O2 production, and LTB4 was again the more potent agonist.

290 esent in the urine of subjects injected with LTB4 was determined using an isotope dilution mass spect

291 LTB4 was unique among 5-lipoxygenase products in this re

292 at the lipid chemoattractant leukotriene B4 (LTB4) was efficacious at causing loss of venular JAM-C a

293 Leukotriene B4 (LTB4) was more potent than cysteinyl LTs.

294 Leukotriene B4 (LTB4) was originally described as a potent lipid myeloid

295 everal glucuronide-conjugated metabolites of LTB4 were characterized including 17-, 18-, 19-, and 20-

296 t investigation, 11 different metabolites of LTB4 were identified in the urine from those subjects in

297 synthesis of proinflammatory leukotriene B4 (LTB4), whereas, in theory, cytoplasmic 5-LOX could favor

298 ory mediators, TNF-alpha and leukotriene B4 (LTB4), which are involved in parasite killing by infecte

299 Co-application of LTB4 with LTA4, LTC4, LTD4, or LTE4 suppressed LTB4-indu

300 uman subjects were injected with 150 nmol/kg LTB4 with one additional subject as placebo control.

301 rat basophilic leukemia RBL-2H3 cells bound LTB4 with similar affinity and activated all of the know

302 tivation and also sequesters leukotriene B4 (LTB4) within an internal binding pocket.