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2 ically active dose of fMLP (5 x 10(-9) M) or leukotriene B(4) (1 x 10(-7) M) in the presence of a phy
3 d miR-219-5p expression along with increased leukotriene B(4) (5-fold) and decreased (~3-fold) specia
4 (FR), platelet-activating factor (PAFR), and leukotriene B(4) (BLTR) were transfected into RBL-2H3 ce
5 whether 15-epi-LXA(4) (anti-inflammatory) or leukotriene B(4) (inflammatory mediator) is produced.
6 ic steps: increased arachidonic acid-derived leukotriene B(4) (LTB(4)) and decreased 5S-hydroxyeicosa
7 k saliva, has dual functions of sequestering leukotriene B(4) (LTB(4)) and inhibiting complement comp
8 te requirement for the lipid chemoattractant leukotriene B(4) (LTB(4)) and its receptor BLT1 for neut
10 ecific binding to human PMN was displaced by leukotriene B(4) (LTB(4)) and LTB(4) receptor 1 (BLT1) a
11 V phospholipase A(2) (hVPLA(2)) could elicit leukotriene B(4) (LTB(4)) biosynthesis in human neutroph
12 inflammatory cell death termed "pyroptosis." Leukotriene B(4) (LTB(4)) is a lipid mediator produced q
20 blished in dogs using ex vivo measurement of leukotriene B(4) (LTB(4)) levels in blood with good corr
23 were complemented by biochemical analyses of leukotriene B(4) (LTB(4)) production and activation of t
25 a lead optimization effort starting with the leukotriene B(4) (LTB(4)) receptor antagonist (2), membe
26 ple chemoattractant receptors, including the leukotriene B(4) (LTB(4)) receptor BLT1 and the chemokin
29 Current immunoassays for the measurement of leukotriene B(4) (LTB(4)) typically utilize an enzyme-li
30 ation of leukotriene synthesis, and produced leukotriene B(4) (LTB(4)) when stimulated with the calci
31 ls, vitamin E forms differentially inhibited leukotriene B(4) (LTB(4)) with an IC(50) of 5-20 muM for
32 catalyzes the final step in the synthesis of leukotriene B(4) (LTB(4)), a potent chemoattractant and
33 tiple Yop effectors can inhibit synthesis of leukotriene B(4) (LTB(4)), a potent lipid mediator relea
35 (cys-LTs), prostaglandin E(2) (PGE(2)), and leukotriene B(4) (LTB(4)), and also 8-isoprostane as a m
37 hil influx, along with cytokines/chemokines, leukotriene B(4) (LTB(4)), and vascular cell adhesion mo
40 r, the role of CXCL1 in mediating neutrophil leukotriene B(4) (LTB(4)), reactive oxygen species (ROS)
41 hibited the formation of the chemoattractant leukotriene B(4) (LTB(4)), specifically in human neutrop
42 LTA(4)H knockdown limited the formation of leukotriene B(4) (LTB(4)), the enzymatic product of LTA(
52 acrophage migration inhibitory factor (MIF), leukotriene B(4) (LTB4), and high mobility group box 1 p
53 activity (p < 0.002) and the chemoattractant leukotriene B(4) (p < 0.02), which fell from a median ba
54 5-oxoprostaglandin 13-reductase, also termed leukotriene B(4) 12-hydroxydehydrogenase (PGR/LTB(4)DH),
57 , GST Mu 5, a hypothetical GST Mu, GST Pi B, leukotriene B(4) 12-hydroxydehydrogenase, and proteasome
58 evels of SPMs and proinflammatory mediators (leukotriene B(4) [LTB(4) ] and prostaglandins) were meas
59 ammatory reactions investigated (elicited by leukotriene B(4) [LTB(4)], CXCL1, tumor necrosis factor
61 zymosan-stimulated PMN showed predominantly leukotriene B(4) and 20-OH-leukotriene B(4), as well as
62 tic increase (>50-fold) in the production of leukotriene B(4) and 5-hydroxyeicosatetraenoic acid, sig
65 bited calcium ionophore-induced leukotriene (leukotriene B(4) and leukotriene C(4)) production, indic
66 l4 deficiency had a significant reduction in leukotriene B(4) and PGE(2) levels in peritoneal exudate
67 ro with the TLR4 agonist, LPS, the levels of leukotriene B(4) and PGE(2) were also significantly decr
69 d lipid inflammatory mediator dihydroxylated Leukotriene B(4) and proresolving mediators such as tri-
71 rgoing apoptosis produced similar amounts of leukotriene B(4) and significantly greater amounts of PG
72 but not Epac-1, suppressed AM production of leukotriene B(4) and TNF-alpha, whereas stimulation of e
74 Z,10E,14Z-eicosatetraenoic acid, and 6-trans-leukotriene B(4) Bioinformatics and experimental approac
75 nd protein excretion) and ex vivo glomerular leukotriene B(4) biosynthesis at 3 hr, and up to 4 days,
76 0 4F3 (CYP4F3) catalyzes the inactivation of leukotriene B(4) by omega-oxidation in human neutrophils
77 date cells showed no detectable responses to leukotriene B(4) confirming the deletion of the BLT1/BLT
78 ine phosphorylation of Vav1, whereas IL-8 or leukotriene B(4) did not, correlating with the requireme
81 ith significant reductions in the release of leukotriene B(4) from stimulated neutrophils and of inte
83 and trachea of Dhrs9(-/-) mice toward 1 muM Leukotriene B(4) is 1.7- to 6-fold lower than that of mi
84 , and trachea of Dhrs9(-/-) mice toward 1 uM Leukotriene B(4) is 1.7- to 6-fold lower than that of mi
90 ls with the chemotactic peptide fMLP or with leukotriene B(4) or fibrinogen results in little increas
92 olic phospholipase A(2) (cPLA(2)) to produce leukotriene B(4) or with cyclooxygenase-2 (COX2) to prod
93 eutrophil fatty acid composition and ex vivo leukotriene B(4) production from stimulated neutrophils
94 its high-affinity G protein-coupled receptor leukotriene B(4) receptor 1 (BLT1) direct dectin-1-depen
95 is study, we report that the LTB(4) receptor leukotriene B(4) receptor 1 (BLT1) redistributes from no
97 ated an important role for the high-affinity leukotriene B(4) receptor BLT1 in arthritis, atheroscler
99 onstrated marked expression of 5-LOX and the leukotriene B(4) receptor in human pancreatic cancer tis
100 (+) monocytes in wild-type mice that express leukotriene B(4) receptor, BLT-1, and that this increase
102 ors with opposing functions, namely ALXR and leukotriene B(4) receptors (BLTs), revealed that the sev
103 of neutrophils, which migrate in response to leukotriene B(4) released by macrophages through 5-lipox
105 crease by approximately 300% in 4 h, whereas leukotriene B(4) stimulated PMN to migrate the full thic
111 ammatory derivatives (prostaglandin E(2) and leukotriene B(4)) and an increased anti-inflammatory der
113 ment in vivo in response to eotaxin, but not leukotriene B(4), a phenomenon that could be prevented b
114 icosatetraenoic acids and, most importantly, leukotriene B(4), an inflammatory mediator involved in l
116 the synovial fluid, TNF-alpha, IL-8, PGE(2), leukotriene B(4), and leukotriene C(4) levels were signi
117 taxis to formylmethionylleucylphenylalanine, leukotriene B(4), and platelet-activating factor was com
118 PG)E(2) and 5-lipoxygenase-derived products, leukotriene B(4), and the biosynthesis interaction produ
119 andin F(2a), prostaglandin D(2) metabolites, leukotriene B(4), and thromboxane levels were lower in s
120 wed predominantly leukotriene B(4) and 20-OH-leukotriene B(4), as well as lipoxin marker 5,15-diHETE.
121 nt by C5a in vivo required amplification via leukotriene B(4), because both C5a-mediated leukocyte re
122 resences of four different chemoattractants (leukotriene B(4), chemokine C-X-C motif ligands 2 and 8,
124 hod allows prostaglandins, thromboxane B(2), leukotriene B(4), hydroxyeicosatetraenoic acid isomers,
126 entrations and was associated with a fall in leukotriene B(4), which is thought to be central to the
127 mponent C5a activates neutrophils to produce leukotriene B(4), which stimulates reactive oxygen speci
128 age activation in vivo and the production of leukotriene B(4), which was required for optimal immune
129 tes (PMN) in vitro chemotaxis in response to leukotriene B(4), with the maximum inhibition ( approxim
130 n of lesional FLAP in myeloid cells promotes leukotriene B(4)-dependent VSMC phenotypic modulation, i
131 y control M-AAT, and significantly decreased leukotriene B(4)-induced neutrophil adhesion (p = 0.04).
132 ally stable LXA(4) analog potently inhibited leukotriene B(4)-induced superoxide anion generation, th