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1 alphaq and is unresponsive to stimulation by leukotriene.
2 macrophages gave higher levels of cysteinyl leukotrienes.
3 issues and excessive production of cysteinyl leukotrienes.
4 th enhanced production of prostaglandins and leukotrienes.
5 e responsiveness of human P2Y12 to cysteinyl leukotrienes.
9 ted leukotriene B4 (LTB4) formation by human leukotriene A4 hydrolase (LTA4H) approximately 40% (P<0.
14 = 0.02), without significant improvement in leukotriene A4 hydrolase activity compared with placebo.
16 agen breakdown with prolyl endopeptidase and leukotriene A4 hydrolase serving as the enzymes responsi
18 dition, FLAP knockdown reduced conversion of leukotriene A4 to leukotriene C4 (LTC4), suggesting a ro
19 ole in the metabolism of arachidonic acid to leukotriene A4, the precursor to the potent pro-inflamma
20 Importantly, we find that neutrophil-derived leukotrienes aid the colonization of distant tissues by
23 protein inhibitor, prevents the synthesis of leukotrienes and 5-oxo-6,8,11,14-eicosatetraenoic acid (
26 horsefly Tabanus yao, has been shown to bind leukotrienes and free fatty acids in vitro Therefore, he
27 farinae through the generation of cysteinyl leukotrienes and proinflammatory cytokines, respectively
28 nificant differences were found according to leukotriene antagonist exposure or whether NSAIDs were r
29 short course of doxycycline (3 weeks), or a leukotriene antagonist may be considered in patients wit
30 f selected asthma controller medication use (leukotriene antagonists and inhaled corticosteroids) on
32 c rhinitis and who then initiated the use of leukotriene antagonists were less likely to experience a
33 icating that pediatric patients treated with leukotriene antagonists were no more likely than those t
38 cosanoids, including prostaglandins (PG) and leukotrienes, are lipid mediators derived from arachidon
39 ing resolvins, lipoxins, prostaglandins, and leukotrienes, as well as leukotriene to resolvin score r
43 ly hypertensive rat (SHR) support a role for leukotriene B4 (LTB4 ), a potent chemoattractant involve
44 ly hypertensive rat (SHR) support a role for leukotriene B4 (LTB4 ), a potent chemoattractant involve
45 ease in the abundance of the proinflammatory leukotriene B4 (LTB4) and a corresponding decrease in th
51 23 activates the synthesis and production of leukotriene B4 (LTB4) in myeloid cells, which modulate i
52 ion has demonstrated the mechanistic role of leukotriene B4 (LTB4) in the molecular pathogenesis of l
56 ith palmitate, enhanced arginase 1 and lower leukotriene B4 (LTB4) levels were detected in macrophage
57 5-lipoxygenase (5-LO) activity and increased leukotriene B4 (LTB4) production have been implicated in
59 e demonstrate that the lipid chemoattractant leukotriene B4 (LTB4) was efficacious at causing loss of
60 )-mediated C5 activation and also sequesters leukotriene B4 (LTB4) within an internal binding pocket.
63 ), and the ratio of SPMs to pro-inflammatory leukotriene B4 (LTB4), are significantly decreased in th
64 ), LXA4, and its counterregulatory compound, leukotriene B4 (LTB4), in patients with childhood asthma
65 X favors the biosynthesis of proinflammatory leukotriene B4 (LTB4), whereas, in theory, cytoplasmic 5
66 ion of inflammatory mediators, TNF-alpha and leukotriene B4 (LTB4), which are involved in parasite ki
71 cosatetraenoic acid, cysteinyl leukotrienes, leukotriene B4 , 11-dehydro-thromboxane B2 , and prostag
72 that BLT2, a G protein-coupled receptor for leukotriene B4 and 12(S)-hydroxyheptadecatrienoic acid (
73 sor to the potent pro-inflammatory mediators leukotriene B4 and leukotriene C4 Studies with small mol
74 spect to inflammatory lipid mediators (i.e., leukotriene B4 and PGs) in omental adipose tissue from O
75 ediators including prostaglandin F2alpha and leukotriene B4 and pro-resolving mediators, including re
76 ectious exudates gave higher proinflammatory leukotriene B4 and procoagulating thromboxane B2, as wel
77 e included inflammation initiating mediators leukotriene B4 and prostaglandin E2 and pro-resolving me
79 n expansion of inflammatory lipid mediators, Leukotriene B4 and Prostaglandin E2, and a concomitant d
80 show that PGE2-G, but not PGE2-EA, inhibits leukotriene B4 biosynthesis, superoxide production, migr
83 the release of high mobility group box 1 and leukotriene B4 from the epithelial cells and this releas
84 Two major G-protein-coupled receptors for leukotriene B4 have been identified: the high-affinity r
85 ic acid, 5-hydroxyeicosatetraenoic acid, and leukotriene B4 in particular could serve as potential bi
86 study, we explored the effect of the C5 and leukotriene B4 inhibitor Ornithodoros moubata complement
87 dimethyl fumarate, phosphodiesterase 4, and leukotriene B4 inhibitors in pemphigoid disorders, and c
93 strategy was applied to a typical GPCR, the leukotriene B4 receptor BLT2, reconstituted in a lipid b
94 this study, we investigated the roles of the leukotriene B4 receptor, BLT1, and CXCR3, the receptor f
95 e lung tumour burden and genetic deletion of leukotriene B4 receptor-1 (BLT1(-/-)) attenuates this in
97 mmunohistochemical analysis showed that both leukotriene B4 receptors were expressed in peripheral se
98 of this defect, as it leads to activation of leukotriene B4 signaling and induction of the alpha4beta
99 covers a previously undefined role of innate leukotriene B4 signaling as a gatekeeper of the hematopo
101 hors show that changing miRNA biogenesis and leukotriene B4 signaling in mice modulates this switch i
103 ic acid, 5-hydroxyeicosatetraenoic acid, and leukotriene B4), TRPV4 (5,6-epoxyeicosatrienoic acid [EE
104 on between rs174537 and the ratio of ARA/LA, leukotriene B4, and 5-HETE but no effect on levels of cy
107 ctions in the generation of pro-inflammatory leukotriene B4, thus LTA4H exhibits opposing pro- and an
116 t cell (MC) mediators (histamine, serotonin, leukotriene C(4), prostaglandin D2, and mouse mast cell
117 Orai3/Orai1 channels are gated by cytosolic leukotriene C4 (LTC4) and require STIM1 downstream LTC4
118 hat airway challenges with the parent CysLT, leukotriene C4 (LTC4), given in combination with low-dos
120 down reduced conversion of leukotriene A4 to leukotriene C4 (LTC4), suggesting a role for the activit
123 idant GSH and the pro-inflammatory cysteinyl leukotriene C4 have been identified as key physiological
126 ro-inflammatory mediators leukotriene B4 and leukotriene C4 Studies with small molecule inhibitors of
131 s were used to test chemotactic responses of leukotriene C4 synthase-deficient and control airway eos
132 -sensitized and ovalbumin aerosol-challenged leukotriene C4 synthase-deficient and control mice.
134 from distal alveolar lung was diminished in leukotriene C4 synthase-deficient mice compared with wil
137 rophages, prostacyclin, prostaglandin E2 and leukotriene C4 were produced within minutes of C. albica
138 rved large conformational changes induced by leukotriene C4, explaining how substrate binding primes
142 activated receptor-2-dependent production of leukotrienes C4 associated with an overexpression of leu
145 F and the generation of histamine, cysteinyl-leukotrienes (cys-LTs) and prostaglandin D(2) (PGD(2) )
147 ough arachidonic acid metabolites, cysteinyl leukotrienes (cys-LTs; leukotriene [LT] C4, LTD4, and LT
149 aluated as Ca2+ flux, secretion of cysteinyl leukotrienes (CysLT), and eosinophil-derived neurotoxin
150 rtner receptors (nucleotide P2Y12, cysteinyl-leukotriene CysLT1) to reconstitute the elusive pharmaco
153 e E4 (LTE4) the most stable of the cysteinyl leukotrienes (cysLTs) binds poorly to classical type 1 (
156 and proinflammatory properties of cysteinyl leukotrienes (cysLTs) in allergic asthma mediate their e
157 irways, involves overproduction of cysteinyl leukotrienes (cysLTs), activation of airway mast cells (
161 r whether lipid mediators, such as cysteinyl leukotrienes (CysLTs), which are present in asthma, coul
163 f both producing and responding to cysteinyl leukotrienes (CystLTs), allowing for the killing of targ
164 sured in purified lung ILC2s stimulated with leukotriene D(4) (LTD(4)) in the presence or absence of
165 sputum eosinophilia correlated with a higher leukotriene D4 (LTD4 ) and leukotriene E4 (LTE4 ) concen
167 red that Galphaq-linked prostaglandin E2 and leukotriene D4 receptors also regulate APP expression.
168 to nematodes, yet are able to undergo robust leukotriene-dependent migration toward IgG-coated beads.
169 report that uracil nucleotides and cysteinyl leukotrienes do not activate human, mouse, or rat GPR17
171 nt of the release of histamine and cysteinyl leukotrienes documented that this bronchoprotective acti
172 ng peripheral airway obstruction and urinary leukotriene E(4) levels indicating cysteinyl leukotriene
173 ICS step-up therapy, whereas higher urinary leukotriene E(4) levels were marginally (P = .053) relat
178 nation of PGD2 and cysLTs (notably cysteinyl leukotriene E4 [LTE4]) enhances TH2 cytokine production.
182 reported outcomes and a reduction in urinary leukotriene E4 levels were observed during roflumilast p
184 Levels of CysLT1R, CysLT2R, and candidate leukotriene E4 receptor P2Y12 mRNAs were increased in IL
185 ysis showed that five biomarkers (20-Hydroxy-leukotriene E4, Lysopc(20:4), 5-methoxytryptamine, Endom
186 ecursors and selectively increased cysteinyl leukotriene formation by mast cells in a manner that was
187 Genetic or pharmacological inhibition of the leukotriene-generating enzyme arachidonate 5-lipoxygenas
191 f a highly influential FADS SNP, rs174537 on leukotriene, HETE, prostaglandin, and thromboxane biosyn
195 viously unrecognized roles for the cysteinyl leukotrienes in regulating the pulmonary trafficking of
198 leukotriene E(4) levels indicating cysteinyl leukotriene inflammation can differentiate LABA step-up
199 differences in the effectiveness of certain leukotriene inhibitors and link the differences in respo
200 ales, but sex as a factor in the response to leukotriene inhibitors has not been fully explored.
201 gets for these diseases and others; however, leukotriene inhibitors have had limited success in the c
203 -,15-hydroxyeicosatetraenoic acid, cysteinyl leukotrienes, leukotriene B4 , 11-dehydro-thromboxane B2
204 model, we observed increased AHR and higher leukotriene levels that were abrogated by anti-PlGF Ab o
212 Cysteinyl leukotrienes (cysLTs), including leukotriene (LT) C4, LTD4, and LTE4, are metabolites of
214 Because fMLP-stimulated neutrophils produce leukotriene (LT)B4, we examined the effect of propofol o
215 ary tetranor prostaglandin (PG)D2 (PGDM) and leukotriene (LT)E4 , induced sputum fluid LTB4 , LTE4 ,
216 ct and is characterized by overproduction of leukotrienes (LT) and large numbers of circulating granu
217 etabolites, cysteinyl leukotrienes (cys-LTs; leukotriene [LT] C4, LTD4, and LTE4), and prostaglandin
219 ame enzymes contributing to the synthesis of leukotrienes LTB4 and LTC4, mediators of inflammation an
222 undant NFAT-dependent role for lipid-derived leukotrienes (LTs) in the activation of lung ILC2s.
223 exhaled breath condensate (EBC) lipoxin and leukotriene measurements can noninvasively characterize
224 re are noted differences in the incidence of leukotriene-mediated diseases in males and females, but
226 PEF data from 493 participants in the LOCCS (Leukotriene Modifier Corticosteroid or Corticosteroid-Sa
228 ng products, inhaled corticosteroids (ICSs), leukotriene modifiers, short-acting beta2-agonists, oral
229 ifferentiating at least five closely related leukotrienes partially coeluting and (almost) unresolvab
231 by a surge in bronchoconstrictory cysteinyl leukotrienes produced at the expense of LTB4 in AERD sub
232 PGs, produced by cyclooxygenases (COX), and leukotrienes, produced by 5-lipoxygenase (5-LO) have bee
233 data reveal that 5-LO, which is required for leukotriene production and subsequent T cell recruitment
234 nematode-derived signals can directly induce leukotriene production by eosinophils and that leukotrie
235 ene C4 synthase (LTC4 S), a key regulator of leukotriene production, could serve as a marker for EoE.
236 rotein in BMDMs was observed, the absence of leukotrienes production reflected an impairment in 5-LO
237 Our data show that LTB4, via its receptor B leukotriene receptor 1 (BLT1) and Galphai signaling, inc
239 rthermore, LTD4 plus PGE2, through cysteinyl leukotriene receptor 1 (CysLT1R) and E-prostanoid recept
241 " neutrophil subset that expressed cysteinyl leukotriene receptor 1 (CysLTR1) and produced TNF, CCL2,
243 d a recurrent mutation in CYSLTR2 (cysteinyl leukotriene receptor 2) encoding a p.Leu129Gln substitut
244 stain cytoplasmic Ca(2+) signaling following leukotriene receptor activation both by refilling the Ca
245 fter rundown of the Ca(2+) signals following leukotriene receptor activation, stimulation of P2Y rece
246 e as a dualistic uracil nucleotide/cysteinyl leukotriene receptor and by others as inactive toward th
247 ccelerated homologous desensitization of the leukotriene receptor and thereby terminated the oscillat
248 steroid (ICS step-up therapy) or addition of leukotriene receptor antagonist (LTRA step-up therapy) o
249 ment with ICSs alone (n = 1758) or ICSs plus leukotriene receptor antagonist (LTRAs; n = 354) or ICSs
250 ge in FEV1 in the Characterizing Response to Leukotriene Receptor Antagonist and Inhaled Corticostero
251 ium Respimat added to ICSs with or without a leukotriene receptor antagonist in a phase III trial in
252 nist, long-acting muscarinic antagonist, and leukotriene receptor antagonist was hospitalized with a
253 vide benefit if combined with montelukast, a leukotriene receptor antagonist, in patients whose sympt
254 he effectiveness of montelukast, a cysteinyl leukotriene receptor antagonist, in the treatment of pos
256 to ICS background therapy, with or without a leukotriene receptor antagonist; long-acting beta2-agoni
257 roids (21.5%; 95% CI: 20.7%-22.3%; p<0.001), leukotriene receptor antagonists (13.4%; 95% CI: 12.9%-1
259 daily inhaled corticosteroids (ICSs), daily leukotriene receptor antagonists, and as-needed ICS trea
260 s, long-acting inhaled beta2-stimulants, and leukotriene receptor antagonists, increased year after y
263 ay disease include the use of muscarinic and leukotriene receptor antagonists; however, these pharmac
264 s the way for future clinical translation of leukotriene receptor inhibition for the treatment of dem
265 This work illustrates that inhibition of leukotriene receptor signalling might represent a safe a
266 enes C4 associated with an overexpression of leukotrienes receptor CysLTR1 by asthmatic BSM cells in
271 kotriene B4 (LTB4R and LTB4R2) and cysteinyl leukotriene receptors (CYSLTR1 and CYSLTR2) contribute t
273 get VEGF receptors but antagonizes cysteinyl leukotriene receptors 1 and 2 (CysLT1-2) at micromolar I
275 ajor findings were: 1) protein levels of all leukotriene receptors were significantly increased in es
276 ing to replenish the PIP2 pool accessible to leukotriene receptors, ostensibly through control of PIP
277 a marketed anti-asthmatic drug antagonizing leukotriene receptors, reduces neuroinflammation, elevat
280 calculated for each patient, and posttrauma leukotriene score to resolvin score ratios were signific
282 ukotriene production by eosinophils and that leukotriene signaling is a major contributor to nematode
285 edin-B (NMB), nerve growth factor (NGF), and leukotriene-synthesis enzymes (ALOX5, ALOX5AP, and LTA4H
286 expression of the Th2 cytokine IL-13 and the leukotriene-synthesizing enzymes 5-lipoxygenase and leuk
288 oids and docosanoids such as prostaglandins, leukotrienes, thromboxanes, isoprostanes, resolvins, hyd
291 tributions of mediators other than cysteinyl leukotrienes to aspirin reactions and to the therapeutic
292 mic Ca(2+) oscillations induced by cysteinyl leukotriene type I receptor activation run down when cel
293 be evoked by modest activation of cysteinyl leukotriene type I receptors by the physiological trigge
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
300 from an imbalance between prostaglandins and leukotrienes, which may serve as targets for future host
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