ライフサイエンスコーパス: leukotriene

1 alphaq and is unresponsive to stimulation by leukotriene.

2 th enhanced production of prostaglandins and leukotrienes.

3 macrophages gave higher levels of cysteinyl leukotrienes.

4 issues and excessive production of cysteinyl leukotrienes.

5 production of proinflammatory and vasoactive leukotrienes.

6 ll mediators histamine (9.0-fold), cysteinyl leukotrienes (4.5-fold), and prostaglandin (PG) D(2) (5.

7 Activation of the leukotriene A(4) hydrolase (LTA(4)H) aminopeptidase (AP)

8 We hypothesized that the genotype of leukotriene A4 hydrolase (encoded by LTA4H), which deter

9 The enzyme leukotriene A4 hydrolase (LTA4H) catalyses the distal st

10 trations, leading to poorer outcomes and (2) leukotriene A4 hydrolase (LTA4H) genotype influenced the

11 roline (PGP) could be degraded by the enzyme leukotriene A4 hydrolase (LTA4H).

12 = 0.02), without significant improvement in leukotriene A4 hydrolase activity compared with placebo.

13 agen breakdown with prolyl endopeptidase and leukotriene A4 hydrolase serving as the enzymes responsi

14 ng inflammation-associated proteins, such as leukotriene A4 hydrolase.

15 ole in the metabolism of arachidonic acid to leukotriene A4, the precursor to the potent pro-inflamma

16 Importantly, we find that neutrophil-derived leukotrienes aid the colonization of distant tissues by

17 Therefore, leukotriene and P2Y receptors utilize distinct membrane

18 We evaluated changes in leukotriene and prostaglandin metabolites for NIUA patie

19 PlGF exacerbates AHR and uniquely links the leukotriene and Th2 pathways in asthma.

20 h tick lipocalins that sequester monoamines, leukotrienes and fatty acids.

21 horsefly Tabanus yao, has been shown to bind leukotrienes and free fatty acids in vitro Therefore, he

22 ids implicated in allergy (such as cysteinyl leukotrienes and prostaglandin D(2)) and the neurotransm

23 o-inflammatory lipid mediators (for example, leukotrienes and prostaglandins) and specialized pro-res

24 the scavenging of proinflammatory cysteinyl leukotrienes and thromboxanes at the feeding site.

25 ions, including phagocytosis, degranulation, leukotriene, and reactive oxygen species (ROS) productio

26 short course of doxycycline (3 weeks), or a leukotriene antagonist may be considered in patients wit

27 Leukotriene antagonists improved nasal symptoms compared

28 Our findings that cysteinyl leukotrienes are involved in regulating airway and lung

29 Leukotrienes are mediators of the innate immune system a

30 Leukotrienes are proinflammatory lipid mediators that ha

31 including prostaglandins, thromboxanes, and leukotrienes, are critical mediators of physiological pr

32 ing resolvins, lipoxins, prostaglandins, and leukotrienes, as well as leukotriene to resolvin score r

33 application to a concise total synthesis of leukotriene B(3).

34 k saliva, has dual functions of sequestering leukotriene B(4) (LTB(4)) and inhibiting complement comp

35 inflammatory cell death termed "pyroptosis." Leukotriene B(4) (LTB(4)) is a lipid mediator produced q

36 blished in dogs using ex vivo measurement of leukotriene B(4) (LTB(4)) levels in blood with good corr

37 tiple Yop effectors can inhibit synthesis of leukotriene B(4) (LTB(4)), a potent lipid mediator relea

38 Receptors for leukotriene B(4) (LTB(4)), prostaglandin E(2) (PGE(2)),

39 hibited the formation of the chemoattractant leukotriene B(4) (LTB(4)), specifically in human neutrop

40 D1 (RvD1) and pro-inflammatory factors, like leukotriene B(4) (LTB(4)).

41 Q0(bolton)-AAT bound IL-8 and leukotriene B(4), comparable to healthy control M-AAT, a

42 y control M-AAT, and significantly decreased leukotriene B(4)-induced neutrophil adhesion (p = 0.04).

43 n of proinflammatory lipid mediators such as leukotriene B(4).

44 in a relative narrow concentration range for leukotriene B4 (100-200 nm).

45 RvE1 binds to leukotriene B4 (BLT-1) on neutrophils and to ERV-1/ChemR

46 ly hypertensive rat (SHR) support a role for leukotriene B4 (LTB4 ), a potent chemoattractant involve

47 ly hypertensive rat (SHR) support a role for leukotriene B4 (LTB4 ), a potent chemoattractant involve

48 ease in the abundance of the proinflammatory leukotriene B4 (LTB4) and a corresponding decrease in th

49 mediated by signaling through the chemokine leukotriene B4 (LTB4) and its receptor LTB4R1.

50 Eicosanoids, such as leukotriene B4 (LTB4) and lipoxin A4 (LXA4), may play a

51 Leukotriene B4 (LTB4) contributes to many inflammatory d

52 23 activates the synthesis and production of leukotriene B4 (LTB4) in myeloid cells, which modulate i

53 ion has demonstrated the mechanistic role of leukotriene B4 (LTB4) in the molecular pathogenesis of l

54 YBB-) neutrophils produced higher amounts of leukotriene B4 (LTB4) in vitro after activation with zym

55 Leukotriene B4 (LTB4) is a major proinflammatory mediato

56 The pro-inflammatory mediator leukotriene B4 (LTB4) is implicated in the pathologies o

57 Leukotriene B4 (LTB4) is secreted by chemotactic neutrop

58 codynamic (PD) relationship based on ex vivo leukotriene B4 (LTB4) levels in dog.

59 ith palmitate, enhanced arginase 1 and lower leukotriene B4 (LTB4) levels were detected in macrophage

60 5-lipoxygenase (5-LO) activity and increased leukotriene B4 (LTB4) production have been implicated in

61 The first potent leukotriene B4 (LTB4) receptor type 2 (BLT2) agonists, e

62 The eicosanoid leukotriene B4 (LTB4) relays chemotactic signals to dire

63 e demonstrate that the lipid chemoattractant leukotriene B4 (LTB4) was efficacious at causing loss of

64 Leukotriene B4 (LTB4), a proinflammatory mediator produc

65 ), and the ratio of SPMs to pro-inflammatory leukotriene B4 (LTB4), are significantly decreased in th

66 ), LXA4, and its counterregulatory compound, leukotriene B4 (LTB4), in patients with childhood asthma

67 ion of inflammatory mediators, TNF-alpha and leukotriene B4 (LTB4), which are involved in parasite ki

68 l-leucyl-phenylalanine (fMLP) is mediated by leukotriene B4 (LTB4).

69 eutrophil production of a second eicosanoid, leukotriene B4 (LTB4).

70 d mediating general neutrophil chemotaxis is leukotriene B4 (LTB4).

71 Leukotriene B4 (LTB4R and LTB4R2) and cysteinyl leukotri

72 g (most notably of the inflammatory mediator leukotriene B4 [LTB4]).

73 that BLT2, a G protein-coupled receptor for leukotriene B4 and 12(S)-hydroxyheptadecatrienoic acid (

74 sor to the potent pro-inflammatory mediators leukotriene B4 and leukotriene C4 Studies with small mol

75 spect to inflammatory lipid mediators (i.e., leukotriene B4 and PGs) in omental adipose tissue from O

76 ediators including prostaglandin F2alpha and leukotriene B4 and pro-resolving mediators, including re

77 ectious exudates gave higher proinflammatory leukotriene B4 and procoagulating thromboxane B2, as wel

78 e included inflammation initiating mediators leukotriene B4 and prostaglandin E2 and pro-resolving me

79 Functionally, aortic Leukotriene B4 and Prostaglandin E2 levels correlated wi

80 n expansion of inflammatory lipid mediators, Leukotriene B4 and Prostaglandin E2, and a concomitant d

81 show that PGE2-G, but not PGE2-EA, inhibits leukotriene B4 biosynthesis, superoxide production, migr

82 Importantly, higher leukotriene B4 concentrations (>0.5 mum) and BLT2 agonis

83 Leukotriene B4 decreased in 4-aminopyridine and EPI grou

84 the release of high mobility group box 1 and leukotriene B4 from the epithelial cells and this releas

85 Two major G-protein-coupled receptors for leukotriene B4 have been identified: the high-affinity r

86 ic acid, 5-hydroxyeicosatetraenoic acid, and leukotriene B4 in particular could serve as potential bi

87 dimethyl fumarate, phosphodiesterase 4, and leukotriene B4 inhibitors in pemphigoid disorders, and c

88 Leukotriene B4 is a proinflammatory lipid mediator whose

89 Inhibition of leukotriene B4 or integrin rescues maturation and migrat

90 pofol binds to 5-lipoxygenase and attenuates leukotriene B4 production.

91 strategy was applied to a typical GPCR, the leukotriene B4 receptor BLT2, reconstituted in a lipid b

92 this study, we investigated the roles of the leukotriene B4 receptor, BLT1, and CXCR3, the receptor f

93 e lung tumour burden and genetic deletion of leukotriene B4 receptor-1 (BLT1(-/-)) attenuates this in

94 Thus, the data show that the two leukotriene B4 receptors have opposing roles in the sens

95 mmunohistochemical analysis showed that both leukotriene B4 receptors were expressed in peripheral se

96 of this defect, as it leads to activation of leukotriene B4 signaling and induction of the alpha4beta

97 covers a previously undefined role of innate leukotriene B4 signaling as a gatekeeper of the hematopo

98 hors show that changing miRNA biogenesis and leukotriene B4 signaling in mice modulates this switch i

99 ic acid, 5-hydroxyeicosatetraenoic acid, and leukotriene B4), TRPV4 (5,6-epoxyeicosatrienoic acid [EE

100 EIA determined leukotriene B4, and ELISAs quantified TNF, IL-12 and IL-

101 migration of PMN toward the chemoattractant leukotriene B4, decreased uptake of L. monocytogenes by

102 into perspective with the data obtained with leukotriene B4, our results illuminate the ligand select

103 Plasma levels of histamine, leukotriene B4, prostaglandin E2, prostaglandin F2, pH,

104 ctions in the generation of pro-inflammatory leukotriene B4, thus LTA4H exhibits opposing pro- and an

105 Accordingly, leukotriene B4-induced thermal hyperalgesia was mediated

106 the amniotic cavity reveals up-regulation of leukotriene B4.

107 Phospholipase A2/5-lipoxygenase/leukotriene-B4 (PLA2/5-LOX/LTB4) axis is an important in

108 5-Lipoxygenase (5-LO) is the key enzyme in leukotriene biosynthesis.

109 and/or GM-CSF, namely, delayed apoptosis and leukotriene biosynthesis.

110 c acid to proinflammatory prostaglandins and leukotrienes by targeting cyclooxygenases (COXs), 5-lipo

111 2) , tetranor-PGE-M, 8-iso-PGF(2) alpha, and leukotriene C(4) , D(4) , and E(4) , were determined usi

112 t cell (MC) mediators (histamine, serotonin, leukotriene C(4), prostaglandin D2, and mouse mast cell

113 trate direct binding of U46619 and cysteinyl leukotrienes C(4), D(4) and E(4) to the P. papatasi prot

114 hat airway challenges with the parent CysLT, leukotriene C4 (LTC4), given in combination with low-dos

115 Cysteinyl leukotrienes (cysLTs), leukotriene C4 (LTC4), LTD4, and LTE4 are proinflammator

116 mation of the proinflammatory lipid mediator leukotriene C4 (LTC4).

117 axis to CCL19 that was restored by exogenous leukotriene C4 .

118 Leukotriene C4 production by mast cells was not enhanced

119 Exogenous administration of leukotriene C4 restored trafficking of eosinophils to pa

120 ro-inflammatory mediators leukotriene B4 and leukotriene C4 Studies with small molecule inhibitors of

121 Leukotriene C4 synthase (LTC4S) catalyzes the formation

122 Hence, inhibition of the leukotriene C4 synthase (LTC4S) enzyme could provide a n

123 mitigated by deletions of either Cysltr2 or leukotriene C4 synthase (Ltc4s).

124 Deletion of leukotriene C4 synthase, the terminal enzyme needed to g

125 s were used to test chemotactic responses of leukotriene C4 synthase-deficient and control airway eos

126 -sensitized and ovalbumin aerosol-challenged leukotriene C4 synthase-deficient and control mice.

127 Leukotriene C4 synthase-deficient eosinophils exhibited

128 from distal alveolar lung was diminished in leukotriene C4 synthase-deficient mice compared with wil

129 f eosinophils to paratracheal lymph nodes in leukotriene C4 synthase-deficient mice.

130 sed retention of eosinophils in the lungs of leukotriene C4 synthase-deficient mice.

131 rved large conformational changes induced by leukotriene C4, explaining how substrate binding primes

132 A with one of its physiological substrates, leukotriene C4.

133 activated receptor-2-dependent production of leukotrienes C4 associated with an overexpression of leu

134 Leukotriene-C4 synthase (LTC4S) generates LTC4 from arac

135 iene-synthesizing enzymes 5-lipoxygenase and leukotriene-C4-synthase.

136 rmacologic inhibition of the proinflammatory leukotriene cascade for therapeutic benefit in early dia

137 Many studies show that the cysteinyl leukotriene cascade remains highly activated in some ast

138 r patients with a highly activated cysteinyl leukotriene cascade.

139 Cysteinyl leukotrienes (cys-LTs) are proinflammatory mediators tha

140 ough arachidonic acid metabolites, cysteinyl leukotrienes (cys-LTs; leukotriene [LT] C4, LTD4, and LT

141 A expression of histamine H(1) and cysteinyl leukotriene CysLT(1) receptors.

142 rtner receptors (nucleotide P2Y12, cysteinyl-leukotriene CysLT1) to reconstitute the elusive pharmaco

143 In contrast, high levels of cysteinyl leukotrienes (cysLTs) and 12-/15-LOX metabolites were pr

144 Cysteinyl leukotrienes (cysLTs) are bronchoconstricting lipid medi

145 Prostaglandin D2 (PGD2) and cysteinyl leukotrienes (cysLTs) are lipid mediators derived from m

146 Cysteinyl leukotrienes (CysLTs) are potent prophlogistic mediators

147 e E4 (LTE4) the most stable of the cysteinyl leukotrienes (cysLTs) binds poorly to classical type 1 (

148 Cysteinyl leukotrienes (cysLTs) facilitate mucosal type 2 immunopa

149 and proinflammatory properties of cysteinyl leukotrienes (cysLTs) in allergic asthma mediate their e

150 e, we show that tuft cells secrete cysteinyl leukotrienes (cysLTs) to rapidly activate type 2 immunit

151 irways, involves overproduction of cysteinyl leukotrienes (cysLTs), activation of airway mast cells (

152 Large amounts of cysteinyl leukotrienes (cysLTs), classically known as a slow react

153 Cysteinyl leukotrienes (cysLTs), including leukotriene (LT) C4, LT

154 The 3 cysteinyl leukotrienes (cysLTs), leukotriene (LT) C(4) (LTC(4)), L

155 Cysteinyl leukotrienes (cysLTs), leukotriene C4 (LTC4), LTD4, and

156 r whether lipid mediators, such as cysteinyl leukotrienes (CysLTs), which are present in asthma, coul

157 e formation of eicosanoids such as cysteinyl leukotrienes (CysLTs).

158 f both producing and responding to cysteinyl leukotrienes (CystLTs), allowing for the killing of targ

159 sed the potency of histamine, carbachol, and leukotriene D(4) as contractile agonists.

160 In vitro stimulation with leukotriene D4 increased iNOS mRNA levels and NO product

161 red that Galphaq-linked prostaglandin E2 and leukotriene D4 receptors also regulate APP expression.

162 report that uracil nucleotides and cysteinyl leukotrienes do not activate human, mouse, or rat GPR17

163 nt of the release of histamine and cysteinyl leukotrienes documented that this bronchoprotective acti

164 metabolite (P < 0.05) and increased urinary leukotriene E(4) (P < 0.01) levels in subjects with aspi

165 eukocyte aggregates, or increases in urinary leukotriene E(4) and prostaglandin D(2) metabolite level

166 Changes in eicosanoid profile (eg, increased leukotriene E(4) level) were limited to patients with N-

167 ng peripheral airway obstruction and urinary leukotriene E(4) levels indicating cysteinyl leukotriene

168 ICS step-up therapy, whereas higher urinary leukotriene E(4) levels were marginally (P = .053) relat

169 Increased production of leukotriene E(4) was restricted to a subgroup of patient

170 ificant aspirin-induced increases in urinary leukotriene E(4), prostaglandin D(2) metabolite, or thro

171 Leukotriene E4 (LTE4) the most stable of the cysteinyl l

172 nation of PGD2 and cysLTs (notably cysteinyl leukotriene E4 [LTE4]) enhances TH2 cytokine production.

173 correlated with basal urinary levels of both leukotriene E4 and PGD-M.

174 d, and quantification of PGD2 metabolite and leukotriene E4 levels was done by using ELISA.

175 reported outcomes and a reduction in urinary leukotriene E4 levels were observed during roflumilast p

176 ant increases in urinary PGD2 metabolite and leukotriene E4 levels.

177 Levels of CysLT1R, CysLT2R, and candidate leukotriene E4 receptor P2Y12 mRNAs were increased in IL

178 ysis showed that five biomarkers (20-Hydroxy-leukotriene E4, Lysopc(20:4), 5-methoxytryptamine, Endom

179 Leukotriene exposure contributes to induction of IRF5 in

180 Cysteinyl leukotriene G protein-coupled receptors CysLT(1) and Cys

181 Genetic or pharmacological inhibition of the leukotriene-generating enzyme arachidonate 5-lipoxygenas

182 ascular permeability, superoxide production, leukotriene generation, leukocyte-induced microvascular

183 eroxide generation, leukocyte adherence, and leukotriene generation.

184 Increased production of leukotrienes has been associated with periodontal diseas

185 Increased production of leukotrienes has been associated with periodontal diseas

186 Leukotrienes have been explored as therapeutic targets f

187 thophysiology of lymphedema, and the role of leukotrienes in lymphedema pathogenesis.

188 levels, 2) FLAP and 5-LOX inhibitors reduce leukotrienes in M1 but less so in M2 macrophages, 3) zil

189 We investigated roles of cysteinyl leukotrienes in mediating eosinophil trafficking from lu

190 viously unrecognized roles for the cysteinyl leukotrienes in regulating the pulmonary trafficking of

191 on of antagonists of histamine and cysteinyl leukotrienes in the presence of indomethacin.

192 ) was demonstrated using a bespoke cysteinyl leukotriene induced rodent model.

193 leukotriene E(4) levels indicating cysteinyl leukotriene inflammation can differentiate LABA step-up

194 loaded with photosensitizers and Zileuton (a leukotriene inhibitor) to obtain MPO and neutrophil targ

195 differences in the effectiveness of certain leukotriene inhibitors and link the differences in respo

196 ales, but sex as a factor in the response to leukotriene inhibitors has not been fully explored.

197 gets for these diseases and others; however, leukotriene inhibitors have had limited success in the c

198 to consideration in the future evaluation of leukotriene inhibitors to treat disease.

199 s and pro-inflammatory lipids (in particular leukotrienes) is strikingly low, providing a molecular e

200 roduction of leukotrienes; we confirmed that leukotriene levels are increased in bronchoalveolar lava

201 model, we observed increased AHR and higher leukotriene levels that were abrogated by anti-PlGF Ab o

202 or 15-LOX-1 inhibitors elevate inflammatory leukotriene levels, 2) FLAP and 5-LOX inhibitors reduce

203 Human leukotriene (LT) A4 hydrolase/aminopeptidase (LTA4H) is

204 The leukotriene (LT) and wingless/integrase (Wnt) pathways h

205 BL/6 mice was associated with high levels of leukotriene (LT) B(4) in the injured alveolus.

206 The 3 cysteinyl leukotrienes (cysLTs), leukotriene (LT) C(4) (LTC(4)), LTD(4), and LTE(4), have

207 mast cells; these assemblies were linked to leukotriene (LT) C(4) production.

208 CTR1 were each produced by human recombinant leukotriene (LT) C(4) synthase (LTC(4)S) and glutathione

209 Cysteinyl leukotrienes (cysLTs), including leukotriene (LT) C4, LTD4, and LTE4, are metabolites of

210 an precision-cut lung slices were exposed to leukotriene (LT) D(4), MCTRs, or both before determinati

211 This was associated with an ablation of leukotriene (LT) production, consistent with production

212 re we define the role of the 5-LO metabolite leukotriene (LT)B(4) and its high-affinity receptor, BLT

213 Because fMLP-stimulated neutrophils produce leukotriene (LT)B4, we examined the effect of propofol o

214 ary tetranor prostaglandin (PG)D2 (PGDM) and leukotriene (LT)E4 , induced sputum fluid LTB4 , LTE4 ,

215 f arachidonic acid (AA)-derived eicosanoids (leukotriene [LT] C(4), prostaglandin [PG] D(2), and thro

216 etabolites, cysteinyl leukotrienes (cys-LTs; leukotriene [LT] C4, LTD4, and LTE4), and prostaglandin

217 Leukotrienes (LTA4, LTB4, LTC4, LTD4, and LTE4) are infl

218 ame enzymes contributing to the synthesis of leukotrienes LTB4 and LTC4, mediators of inflammation an

219 s is extremely rapid and faster than that of leukotriene (LTE(4)).

220 Proinflammatory leukotrienes (LTs) are produced by 5-lipoxygenase (5-LO)

221 Leukotrienes (LTs) are proinflammatory lipid mediators f

222 undant NFAT-dependent role for lipid-derived leukotrienes (LTs) in the activation of lung ILC2s.

223 , produce either abundant prostaglandins and leukotrienes (M1) or SPMs (M2).

224 re are noted differences in the incidence of leukotriene-mediated diseases in males and females, but

225 th their classic substrates in the cysteinyl leukotriene metabolome.

226 PEF data from 493 participants in the LOCCS (Leukotriene Modifier Corticosteroid or Corticosteroid-Sa

227 Increased use of ICSs and leukotriene modifiers was observed just after the regula

228 ng products, inhaled corticosteroids (ICSs), leukotriene modifiers, short-acting beta2-agonists, oral

229 SPM levels without affecting proinflammatory leukotrienes or PGs.

230 ifferentiating at least five closely related leukotrienes partially coeluting and (almost) unresolvab

231 Pharmacologic blockade of the leukotriene pathway holds potential as a novel therapy t

232 Plgf-/- mice treated with leukotrienes phenocopied the WT response to allergen exp

233 PGs, produced by cyclooxygenases (COX), and leukotrienes, produced by 5-lipoxygenase (5-LO) have bee

234 data reveal that 5-LO, which is required for leukotriene production and subsequent T cell recruitment

235 roven to attenuate 5-LO pathway activity and leukotriene production in human clinical trials.

236 ependent and greater than 90% suppression of leukotriene production over 24 h.

237 Here, we show that HMGB1 induces leukotriene production through a RAGE-dependent pathway,

238 rotein in BMDMs was observed, the absence of leukotrienes production reflected an impairment in 5-LO

239 Antagonists of the type 1 cysteinyl leukotriene receptor (CysLT1R) are widely used to treat

240 Our data show that LTB4, via its receptor B leukotriene receptor 1 (BLT1) and Galphai signaling, inc

241 B4 act through activation of its receptor, B leukotriene receptor 1 (BLT1).

242 rthermore, LTD4 plus PGE2, through cysteinyl leukotriene receptor 1 (CysLT1R) and E-prostanoid recept

243 " neutrophil subset that expressed cysteinyl leukotriene receptor 1 (CysLTR1) and produced TNF, CCL2,

244 and montelukast, an antagonist of cysteinyl leukotriene receptor 1.

245 ing the G protein-coupled receptor cysteinyl-leukotriene receptor 2 (CysLTR2).

246 d a recurrent mutation in CYSLTR2 (cysteinyl leukotriene receptor 2) encoding a p.Leu129Gln substitut

247 stain cytoplasmic Ca(2+) signaling following leukotriene receptor activation both by refilling the Ca

248 fter rundown of the Ca(2+) signals following leukotriene receptor activation, stimulation of P2Y rece

249 e as a dualistic uracil nucleotide/cysteinyl leukotriene receptor and by others as inactive toward th

250 Leukotriene receptor antagonism resulted in a significan

251 ment with ICSs alone (n = 1758) or ICSs plus leukotriene receptor antagonist (LTRAs; n = 354) or ICSs

252 edication (long-acting beta2-agonist [LABA], leukotriene receptor antagonist [LTRA], theophylline, or

253 treatment with H1 and H2 receptor blockers, leukotriene receptor antagonist and consideration for pr

254 ium Respimat added to ICSs with or without a leukotriene receptor antagonist in a phase III trial in

255 nist, long-acting muscarinic antagonist, and leukotriene receptor antagonist was hospitalized with a

256 mouse model, we administered montelukast, a leukotriene receptor antagonist, and diabetes-related re

257 vide benefit if combined with montelukast, a leukotriene receptor antagonist, in patients whose sympt

258 he effectiveness of montelukast, a cysteinyl leukotriene receptor antagonist, in the treatment of pos

259 ceptor antagonist, cetirizine, and cysteinyl-leukotriene receptor antagonist, montelukast, as well as

260 ecommend an intranasal corticosteroid over a leukotriene receptor antagonist.

261 to ICS background therapy, with or without a leukotriene receptor antagonist; long-acting beta2-agoni

262 Long-acting beta2-agonists (LABA) and leukotriene receptor antagonists (LTRA) are two principa

263 daily inhaled corticosteroids (ICSs), daily leukotriene receptor antagonists, and as-needed ICS trea

264 ticosteroids, long-acting beta-agonists, and leukotriene receptor antagonists.

265 ay disease include the use of muscarinic and leukotriene receptor antagonists; however, these pharmac

266 The low affinity leukotriene receptor BLT2 is a receptor involved in pro-

267 s the way for future clinical translation of leukotriene receptor inhibition for the treatment of dem

268 This work illustrates that inhibition of leukotriene receptor signalling might represent a safe a

269 enes C4 associated with an overexpression of leukotrienes receptor CysLTR1 by asthmatic BSM cells in

270 Finally, leukotrienes receptor expression was assessed in vitro b

271 Leukotriene-receptor antagonists (LTRAs) are recommended

272 Leukotriene-receptor antagonists as monotherapy improved

273 Leukotriene-receptor antagonists either as monotherapy o

274 kotriene B4 (LTB4R and LTB4R2) and cysteinyl leukotriene receptors (CYSLTR1 and CYSLTR2) contribute t

275 genic small molecule antagonist of cysteinyl leukotriene receptors 1 and 2 (CysLT1 and CysLT2).

276 get VEGF receptors but antagonizes cysteinyl leukotriene receptors 1 and 2 (CysLT1-2) at micromolar I

277 The expression of leukotriene receptors was deregulated in esophageal squa

278 ajor findings were: 1) protein levels of all leukotriene receptors were significantly increased in es

279 ing to replenish the PIP2 pool accessible to leukotriene receptors, ostensibly through control of PIP

280 a marketed anti-asthmatic drug antagonizing leukotriene receptors, reduces neuroinflammation, elevat

281 actor that acts on plasma membrane cysteinyl leukotriene receptors.

282 calculated for each patient, and posttrauma leukotriene score to resolvin score ratios were signific

283 higher resolvin scores (p < 0.001) and lower leukotriene scores (p < 0.001).

284 However, mice deficient in leukotriene signaling show markedly attenuated eosinophi

285 te ILC2s, and tuft-cell-specific ablation of leukotriene synthesis attenuates type 2 immunity and del

286 edin-B (NMB), nerve growth factor (NGF), and leukotriene-synthesis enzymes (ALOX5, ALOX5AP, and LTA4H

287 expression of the Th2 cytokine IL-13 and the leukotriene-synthesizing enzymes 5-lipoxygenase and leuk

288 osinophils, and macrophages, creating a PlGF/leukotriene/Th2-response positive feedback loop.

289 oids and docosanoids such as prostaglandins, leukotrienes, thromboxanes, isoprostanes, resolvins, hyd

290 prostaglandins, and leukotrienes, as well as leukotriene to resolvin score ratios.

291 s, stimulate tuft cells to release cysteinyl leukotrienes to amplify anti-helminth immunity in the sm

292 tributions of mediators other than cysteinyl leukotrienes to aspirin reactions and to the therapeutic

293 mic Ca(2+) oscillations induced by cysteinyl leukotriene type I receptor activation run down when cel

294 airways challenged by noninjurious histamine-leukotriene-type autacoids also respond through prompt m

295 ALOX5 is essential for the production of leukotrienes; we confirmed that leukotriene levels are i

296 nzyme of the biosynthesis of proinflammatory leukotrienes were in the range of the approved drug zile

297 poxygenase (5-LO) is key in the synthesis of leukotrienes, which are potent proinflammatory lipid med

298 LTC4 is the parent molecule of the cysteinyl leukotrienes, which are recognized for their pathogenic

299 f bioactive mediators, such as histamine and leukotrienes, which initiate allergic reactions.

300 from an imbalance between prostaglandins and leukotrienes, which may serve as targets for future host