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1 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
2 d miR-219-5p expression along with increased leukotriene B(4) (5-fold) and decreased (~3-fold) specia
3 (FR), platelet-activating factor (PAFR), and leukotriene B(4) (BLTR) were transfected into RBL-2H3 ce
4 whether 15-epi-LXA(4) (anti-inflammatory) or leukotriene B(4) (inflammatory mediator) is produced.
5 ic steps: increased arachidonic acid-derived leukotriene B(4) (LTB(4)) and decreased 5S-hydroxyeicosa
6 te requirement for the lipid chemoattractant leukotriene B(4) (LTB(4)) and its receptor BLT1 for neut
7                                              Leukotriene B(4) (LTB(4)) and leukotriene C(4) (LTC(4))
8 ecific binding to human PMN was displaced by leukotriene B(4) (LTB(4)) and LTB(4) receptor 1 (BLT1) a
9 V phospholipase A(2) (hVPLA(2)) could elicit leukotriene B(4) (LTB(4)) biosynthesis in human neutroph
10                                              Leukotriene B(4) (LTB(4)) is a potent chemoattractant ac
11                                              Leukotriene B(4) (LTB(4)) is a potent chemoattractant fo
12                                              Leukotriene B(4) (LTB(4)) is a potent lipid mediator of
13                                              Leukotriene B(4) (LTB(4)) is a potent proinflammatory li
14                                              Leukotriene B(4) (LTB(4)) is a potent, proinflammatory m
15                                              Leukotriene B(4) (LTB(4)) is a pro-inflammatory mediator
16                                              Leukotriene B(4) (LTB(4)) is a product of eicosanoid met
17                                              Leukotriene B(4) (LTB(4)) mediates a variety of inflamma
18                                              Leukotriene B(4) (LTB(4)) receptor (BLT)1 is expressed o
19 a lead optimization effort starting with the leukotriene B(4) (LTB(4)) receptor antagonist (2), membe
20 ple chemoattractant receptors, including the leukotriene B(4) (LTB(4)) receptor BLT1 and the chemokin
21                                          PMN leukotriene B(4) (LTB(4)) synthesis was also augmented a
22  Current immunoassays for the measurement of leukotriene B(4) (LTB(4)) typically utilize an enzyme-li
23 ation of leukotriene synthesis, and produced leukotriene B(4) (LTB(4)) when stimulated with the calci
24 ls, vitamin E forms differentially inhibited leukotriene B(4) (LTB(4)) with an IC(50) of 5-20 muM for
25 catalyzes the final step in the synthesis of leukotriene B(4) (LTB(4)), a potent chemoattractant and
26                  Current models propose that leukotriene B(4) (LTB(4)), a secondary chemoattractant s
27  (cys-LTs), prostaglandin E(2) (PGE(2)), and leukotriene B(4) (LTB(4)), and also 8-isoprostane as a m
28 factor (PAF), interleukin-8 (IL-8), C5a, and leukotriene B(4) (LTB(4)), and it was normal.
29 hil influx, along with cytokines/chemokines, leukotriene B(4) (LTB(4)), and vascular cell adhesion mo
30                                              Leukotriene B(4) (LTB(4)), interacting with its high-aff
31 r, the role of CXCL1 in mediating neutrophil leukotriene B(4) (LTB(4)), reactive oxygen species (ROS)
32   LTA(4)H knockdown limited the formation of leukotriene B(4) (LTB(4)), the enzymatic product of LTA(
33              We have recently shown that the leukotriene B(4) (LTB(4))-BLT1 pathway is important in e
34 ctive oxygen species, and the lipid mediator leukotriene B(4) (LTB(4)).
35 he inflammatory mediator and chemoattractant leukotriene B(4) (LTB(4)).
36 yme that generates the inflammatory mediator leukotriene B(4) (LTB(4)).
37           Similar results were obtained with leukotriene B(4) (LTB(4)).
38 l mucosal injury and decreased generation of leukotriene B(4) (LTB(4)).
39 acrophage migration inhibitory factor (MIF), leukotriene B(4) (LTB4), and high mobility group box 1 p
40 activity (p < 0.002) and the chemoattractant leukotriene B(4) (p < 0.02), which fell from a median ba
41 5-oxoprostaglandin 13-reductase, also termed leukotriene B(4) 12-hydroxydehydrogenase (PGR/LTB(4)DH),
42                     It is also known for its leukotriene B(4) 12-hydroxydehydrogenase activity.
43  decreased levels of mRNA encoding GST Mu 1, leukotriene B(4) 12-hydroxydehydrogenase, and LMP7.
44 , GST Mu 5, a hypothetical GST Mu, GST Pi B, leukotriene B(4) 12-hydroxydehydrogenase, and proteasome
45 ammatory reactions investigated (elicited by leukotriene B(4) [LTB(4)], CXCL1, tumor necrosis factor
46            The 5-lipoxygenase (5LO) produces leukotriene B(4) and 15-epilipoxin-A(4) (15-epi-LXA(4)).
47  zymosan-stimulated PMN showed predominantly leukotriene B(4) and 20-OH-leukotriene B(4), as well as
48 tic increase (>50-fold) in the production of leukotriene B(4) and 5-hydroxyeicosatetraenoic acid, sig
49     The major metabolites of AA made by PMN, leukotriene B(4) and 5-hydroxyicosatetraenoate, did not
50  which also catalyzes omega-hydroxylation of leukotriene B(4) and arachidonic acid.
51 bited calcium ionophore-induced leukotriene (leukotriene B(4) and leukotriene C(4)) production, indic
52 ularly N-formylated tripeptides and possibly leukotriene B(4) and platelet activating factor.
53 x 10(5) cells; P < .01) and lower amounts of leukotriene B(4) and prostaglandin than M1.
54 rgoing apoptosis produced similar amounts of leukotriene B(4) and significantly greater amounts of PG
55  but not Epac-1, suppressed AM production of leukotriene B(4) and TNF-alpha, whereas stimulation of e
56 6-fold higher than the K(m) of CYP4F3A using leukotriene B(4) as a substrate.
57 nd protein excretion) and ex vivo glomerular leukotriene B(4) biosynthesis at 3 hr, and up to 4 days,
58 0 4F3 (CYP4F3) catalyzes the inactivation of leukotriene B(4) by omega-oxidation in human neutrophils
59 date cells showed no detectable responses to leukotriene B(4) confirming the deletion of the BLT1/BLT
60 ine phosphorylation of Vav1, whereas IL-8 or leukotriene B(4) did not, correlating with the requireme
61                                   PGE(2) and leukotriene B(4) each enhanced development of periodonti
62                             The synthesis of leukotriene B(4) from arachidonic acid requires the sequ
63 ith significant reductions in the release of leukotriene B(4) from stimulated neutrophils and of inte
64 y for hypoxia-induced lipid peroxidation and leukotriene B(4) generation.
65                                              Leukotriene B(4) is a proinflammatory lipid mediator gen
66 tazone plus atorvastatin plus H-89 increased leukotriene B(4) levels.
67            Neutrophil production of IL-1 and leukotriene B(4) likely contributes to inflammation but
68                                              Leukotriene B(4) mediates diverse inflammatory diseases
69  did not significantly reduce NCA induced by leukotriene B(4) or complement-activated serum.
70 ls with the chemotactic peptide fMLP or with leukotriene B(4) or fibrinogen results in little increas
71 fically prolonged in response to PAF but not leukotriene B(4) or N-formyl-Met-Leu-Phe.
72 olic phospholipase A(2) (cPLA(2)) to produce leukotriene B(4) or with cyclooxygenase-2 (COX2) to prod
73 eutrophil fatty acid composition and ex vivo leukotriene B(4) production from stimulated neutrophils
74 its high-affinity G protein-coupled receptor leukotriene B(4) receptor 1 (BLT1) direct dectin-1-depen
75 is study, we report that the LTB(4) receptor leukotriene B(4) receptor 1 (BLT1) redistributes from no
76                             RvE1 through the leukotriene B(4) receptor BLT1 enhanced NADPH oxidase-de
77 ated an important role for the high-affinity leukotriene B(4) receptor BLT1 in arthritis, atheroscler
78                                          One leukotriene B(4) receptor has been recently identified (
79 onstrated marked expression of 5-LOX and the leukotriene B(4) receptor in human pancreatic cancer tis
80 (+) monocytes in wild-type mice that express leukotriene B(4) receptor, BLT-1, and that this increase
81                         BLT2, a low-affinity leukotriene B(4) receptor, was also shown to be a high-a
82 ors with opposing functions, namely ALXR and leukotriene B(4) receptors (BLTs), revealed that the sev
83                                              Leukotriene B(4) signals primarily through its high-affi
84 crease by approximately 300% in 4 h, whereas leukotriene B(4) stimulated PMN to migrate the full thic
85 iae and reduced calcium-ionophore-stimulated leukotriene B(4) synthesis in vitro.
86 , alveolar macrophage bacterial killing, and leukotriene B(4) synthesis.
87 apacity of stimulated neutrophils to produce leukotriene B(4) was decreased by 31%.
88                                              Leukotriene B(4) was down-regulated in M2 (668 +/- 81 vs
89  induced in the joints, and the 5-LO product leukotriene B(4) was produced.
90 ammatory derivatives (prostaglandin E(2) and leukotriene B(4)) and an increased anti-inflammatory der
91 nce of ciprofibrate, a synthetic ligand, and leukotriene B(4), a natural ligand.
92 ment in vivo in response to eotaxin, but not leukotriene B(4), a phenomenon that could be prevented b
93 icosatetraenoic acids and, most importantly, leukotriene B(4), an inflammatory mediator involved in l
94 ptide-78, granulocyte chemotactic protein-2, leukotriene B(4), and FMLP.
95 the synovial fluid, TNF-alpha, IL-8, PGE(2), leukotriene B(4), and leukotriene C(4) levels were signi
96 taxis to formylmethionylleucylphenylalanine, leukotriene B(4), and platelet-activating factor was com
97 PG)E(2) and 5-lipoxygenase-derived products, leukotriene B(4), and the biosynthesis interaction produ
98 wed predominantly leukotriene B(4) and 20-OH-leukotriene B(4), as well as lipoxin marker 5,15-diHETE.
99 nt by C5a in vivo required amplification via leukotriene B(4), because both C5a-mediated leukocyte re
100 resences of four different chemoattractants (leukotriene B(4), chemokine C-X-C motif ligands 2 and 8,
101 hod allows prostaglandins, thromboxane B(2), leukotriene B(4), hydroxyeicosatetraenoic acid isomers,
102 entrations and was associated with a fall in leukotriene B(4), which is thought to be central to the
103 age activation in vivo and the production of leukotriene B(4), which was required for optimal immune
104 tes (PMN) in vitro chemotaxis in response to leukotriene B(4), with the maximum inhibition ( approxim
105 n of lesional FLAP in myeloid cells promotes leukotriene B(4)-dependent VSMC phenotypic modulation, i
106 ally stable LXA(4) analog potently inhibited leukotriene B(4)-induced superoxide anion generation, th
107         RvD1 and RvD2 each reduced MCP-1 and leukotriene B(4)-stimulated monocyte adhesion to adipocy
108 duce VSMC migration ex vivo was rescued with leukotriene B(4).
109  PtdIns are hydroxyeicosatetraenoic acids or leukotriene B(4).
110 oxins and hyperinflammation driven by excess leukotriene B(4).
111 e chemoattractants of fMLP > CXCL8 > CXCL2 > leukotriene B(4).
112  MPhi efferocytosis, an action not shared by leukotriene B(4).
113 d neutrophil and monocyte trafficking toward leukotriene B(4).
114  receptors for the 5-lipoxygenase metabolite leukotriene B(4).
115  with structurally related lipids PGE(2) and leukotriene B(4).
116 ion and PD1/NPD1 levels as well as decreased leukotriene B(4).
117 whereas it was normal in response to IL-8 or leukotriene B(4).
118 receptor of the downstream 5-LOX metabolite, leukotriene B(4).
119 eutrophil chemoattractants interleukin-8 and leukotriene B(4).
120 ing in the conversion of arachidonic acid to leukotriene B(4).
121 vity and tumor regression were suppressed in leukotriene B(4)R-deficient (BLT-1(-/-)) mice.
122                                  We measured leukotriene-B(4) (LTB(4)) and LTC(4)/D(4)/E(4), inflamma
123                 Conversely, whereas IL-8 and leukotriene-B(4)-mediated transmigration is PECAM-1-inde

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