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 phil adhesion and degranulation responses to LTB4.

7 involving amplified neutrophil production of LTB4.

8 insulin sensitization, possibly by reducing LTB4.

9 e site, probably preventing tight docking of LTB4.

10 he formation of the proinflammatory mediator LTB4.

11 zation with the neutrophil chemotactic agent LTB4.

12 red engagement of receptors for both MIF and LTB4.

13 d BLT2 mRNA and inhibited their migration to LTB4.

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

15 before intraluminal injection of toxin A or LTB4.

16 ls by lymph node neutrophils is initiated by LTB4.

17 of the inflammatory mediator leukotriene B4 [LTB4]).

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

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

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

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

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

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

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

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

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

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

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

29 LTB4 also stimulated TRPV1-mediated substance P release

30 1 selectively blocks conversion of LTA4 into LTB4, although sparing the enzyme's anti-inflammatory am

31 LTB4 and block of the LTB4-stimulated increase in [Ca(2+

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

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

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

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

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

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

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

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

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

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

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

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

44 uction by primary neutrophils in response to LTB4 and MIP-2 and in the migration of neutrophils durin

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

46 4 and PGE2, whereas the relationship between LTB4 and PGE2 was not as strong.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

62 pared with WT cells, and the effect was also LTB4- and BLT1-dependent.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

89 However, the mechanisms by which the LTB4-BLT1 axis relays chemotactic signals during intrava

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

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

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

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

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

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

96 We conclude that LTB4/BLT1 signaling has an unexpected critical role in m

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

98 oth RvE1 and RvD1 receptors directly inhibit LTB4 by phosphorylating the LTB4 receptor using beta adr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

119 Furthermore, LTB4 decreased insulin receptor tyrosine phosphorylation

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

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

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

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

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

125 vital subcellular microscopy, we reveal that LTB4 elicits sustained cell polarization and adhesion re

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

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

128 LTB4 failed to activate beta1 subunit-containing channel

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

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

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

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

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

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

135 This study identifies neutrophil LTB4 generation as a target of NADPH oxidase regulation,

136 Increased LTB4 generation by CGD neutrophils was also augmented by

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

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

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

140 mechanism that regulates the development of LTB4 gradients.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

157 s produced higher amounts of leukotriene B4 (LTB4) in vitro after activation with zymosan or immune c

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

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

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

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

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

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

164 The actions of RvE1 on LTB4-induced [Ca(2+)](i) increase were reversed by siRNA

165 whereas RvD1 receptor only counterregulates LTB4-induced [Ca(2+)](i) increase.

166 vD1 for 30 minutes significantly blocked the LTB4-induced [Ca(2+)](i) increase.

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

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

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

170 RvE1, but not RvD1, counterregulated the LTB4-induced high-molecular-weight glycoprotein secretio

171 RvE1 receptor counterregulates the LTB4-induced increase in [Ca(2+)](i) and secretion, wher

172 1 receptors but not LTB4 receptors inhibited LTB4-induced inflammation.

173 ermined the actions of both RvE1 and RvD1 on LTB4-induced responses of goblet cells cultured from rat

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

180 While LTB4 is involved in adipose tissue inflammation and insu

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

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

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

184 Leukotriene B4 (LTB4) is a major proinflammatory mediator important in h

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

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

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

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

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

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

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

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

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

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

195 ared with WT mice and associated with higher LTB4 levels.

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

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

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

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

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

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

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

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

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

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

206 tion of extracellular vesicle release blocks LTB4-mediated autocrine/paracrine signaling required for

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

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

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

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

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

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

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

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

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

224 Here, we report that LTB4 produced by neutrophils acts as an autocrine/paracr

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

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

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

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

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

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

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

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

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

234 ce neutrophil activation, degranulation, and LTB4 production.

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

236 5-LO) activity and increased leukotriene B4 (LTB4) production have been implicated in various inflamm

237 4 (15-epi-LXA4), lipoxin A4, leukotriene B4 (LTB4), prostaglandin E2 (PGE2), and interleukin (IL)-6 a

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

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

240 ould be targeted by inhibitors of the LTB(4)-LTB4 receptor 1 (BLT1) pathway as a novel therapeutic ap

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

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

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

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

245 o augmented by paracrine cross talk with 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 directly inhibit LTB4 by phosphorylating the LTB4 receptor using beta adrenergic receptor kinase.

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

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

254 The first potent leukotriene B4 (LTB4) receptor type 2 (BLT2) agonists, endogenous 12(S)-

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

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

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

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

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

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

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

262 ver a novel complementary mechanism by which LTB4 relays extravasation signals in neutrophils during

263 The eicosanoid leukotriene B4 (LTB4) relays chemotactic signals to direct neutrophil mi

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

265 irectional motility with concomitant loss of LTB4 release.

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

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

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

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

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

271 Specifically, LTB4 signaling coordinates the dynamic redistribution of

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

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

274 LTB4 signaling is not required for migration to HXA3 sig

275 LTB4 and block of the LTB4-stimulated increase in [Ca(2+)](i) by RvE1 and RvD1

276 The RvE1 and RvD1 block of LTB4-stimulated increase in [Ca(2+)](i) was also reverse

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

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

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

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

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

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

283 Pharmacologic blockade of LTB4 synthesis inhibited allergic skin inflammation elic

284 Inhibiting LTB4 synthesis or antagonizing the BLT1 receptor after z

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

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

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

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

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

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

291 LTB4 triggered SMC chemotaxis, which was pertussis toxin

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

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

294 Thus, LTB4 was the major driver of excessive neutrophilic lung

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

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

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