ライフサイエンスコーパス: lipoxin

1 ing nature's own anti-inflammatory molecule, lipoxin.

2 the production of resolvins, protectins, and lipoxins.

3 resolving mediators, including resolvins and lipoxins.

4 uired for synthesis of the anti-inflammatory lipoxins.

5 g eicosanoid substrates to anti-inflammatory lipoxins.

6 rocessing, was attenuated in the presence of lipoxins.

7 in severe asthma include underproduction of lipoxins.

8 s are classified as aspirin-triggered 15-epi-lipoxins.

9 ive lipid mediators such as leukotrienes and lipoxins.

10 nals provided by a class of molecules called lipoxins.

11 valuating the therapeutic potential of using lipoxins.

12 pacity for antiinflammatory and proresolving lipoxins.

13 ors blocked LTC4 and increased resolvins and lipoxins.

14 vel possibility for treating KS and PEL with lipoxins.

15 5-LOX into epimeric lipoxins, termed 15-epi-lipoxins (15-epi-lipoxin A4 [e-LXA4]).

16 In addition, we compared the effects of lipoxin A(4) (100 nM) with vehicle on basal and LPS-stim

17 We also show that aspirin-triggered 15-epi-lipoxin A(4) (15-epi-LXA(4)) and 17-epi-resolvin D1 (17-

18 uced by tendon-derived stromal cells, 15-epi-Lipoxin A(4) (15-epi-LXA(4)) or maresin (MaR)-1, moderat

19 10(5) cells; P < .01), whereas SPM including lipoxin A(4) (977 +/- 173 vs 675 +/- 167 pg/2.5 x 10(5)

20 In this study, we report that synthetic lipoxin A(4) (LXA(4)) and 15-epi-LXA(4) (i.e., 15(R)-LXA

21 Lipoxin A(4) (LXA(4)) and aspirin-triggered 15-epi-LXA(4

22 Lipoxin A(4) (LXA(4)) and docosahexaenoic acid-derived n

23 dins E(2) (PGE(2)), F(2alpha) (PGF(2alpha)), lipoxin A(4) (LXA(4)) and its receptor FPR2/ALX were ana

24 X-2)-derived prostaglandin E(2) (PGE(2)) and lipoxin A(4) (LXA(4)) as pivotal mediators in vivo for r

25 Lipoxin A(4) (LXA(4)) can also interact with ALX/FPR2 re

26 ects of PRP on monocyte cytokine release and lipoxin A(4) (LXA(4)) generation.

27 The eicosanoid lipoxin A(4) (LXA(4)) has emerging roles in lymphocyte-d

28 Lipoxin A(4) (LXA(4)) is a structurally and functionally

29 the effect of pro-inflammatory mediators on lipoxin A(4) (LXA(4)) production and FPR2/ALX expression

30 a synthetic nonpsychoactive cannabinoid, and lipoxin A(4) (LXA(4)), an eicosanoid formed from sequent

31 By inducing production of lipoxin A(4) (LXA(4)), which blocks PGE(2) biosynthesis,

32 s 15-lipoxygenase (15-LOX) and receptors for lipoxin A(4) (LXA(4)), which have been implicated in an

33 Lipoxin A(4) also reduced the elastase release from homo

34 Moreover, aspirin-triggered lipoxin A(4) analog evoked release of the antiphlogistic

35 Also, aspirin-triggered lipoxin A(4) analog markedly inhibited proinflammatory c

36 For example, aspirin-triggered lipoxin A(4) analog reduced Psi(max), resolvin E1 decrea

37 Administration of aspirin-triggered lipoxin A(4) analog, resolvin E1, or 10,17S-docosatriene

38 ontaining aspirin-triggered resolvin D1 or a lipoxin A(4) analog.

39 rate for the first time a potential role for lipoxin A(4) and its receptor in the resolution of the i

40 ds natural and synthetic peptides as well as lipoxin A(4) and mediates important biological functions

41 We measured serum levels of lipoxin A(4) and myometrial protein release using ELISA,

42 We found that lipoxin A(4) and resolvin D1, in solution or incorporate

43 ediated pathway stimulates the production of lipoxin A(4) as well as other signaling molecules called

44 he lipid derivatives resolving D1 and D2 and lipoxin A(4) attenuated HLMC histamine release in a dose

45 In addition, lipoxin A(4) displayed a CB(1) receptor-dependent protec

46 emaining; synthesis of the anti-inflammatory lipoxin A(4) from arachidonic acid is also detected.

47 d on ultrastructural analysis, IL-8 release, lipoxin A(4) generation, mucin production, and lipoxygen

48 n wild-type mice but both aspirin and 15-epi-lipoxin A(4) had markedly reduced effects on leukocyte-e

49 Levels of lipoxin A(4) in nonpregnant women were 0.48 +/- 0.04 nM,

50 ere we show that the anti-inflammatory lipid lipoxin A(4) is an endogenous allosteric enhancer of the

51 the effects of 15-epi-16-(p-fluoro)-phenoxy-lipoxin A(4) methyl ester, an aspirin-triggered lipoxin

52 trast, the specialized proresolving mediator lipoxin A(4) promoted NK cell LIMK expression, lytic gra

53 In addition, the Lipoxin A(4) receptor (FPR2/ALX) was used as marker for

54 We report that the lipoxin A(4) receptor is expressed on spinal astrocytes

55 ceptors for RvD1 gave two candidates--ALX, a lipoxin A(4) receptor, and GPR32, an orphan--that were c

56 15-lipoxygenase (15-LOX) and lipoxin A(4) receptors (ALX) constitute a LXA(4) circuit

57 nistrations of a synthetic aspirin-triggered lipoxin A(4) signal mimetic, ATLa, to probe dynamics of

58 Lipoxin A(4) significantly reduced LPS-induced but not b

59 ased more IL-8, and produced lower levels of lipoxin A(4) than that from patients with mild asthma.

60 Mean +/- SE circulating level of lipoxin A(4) was 5.89 +/- 0.63 nM at 24-wk gestation, wi

61 Lipoxin A(4) was detected in brain tissues, did not comp

62 Aspirin and 15-epi-lipoxin A(4) were shown to inhibit leukocyte trafficking

63 ecessary for NK cell cytotoxicity, including lipoxin A(4)'s proresolving actions.

64 by the proresolving lipoxygenase metabolite, lipoxin A(4), a potent stop signal.

65 of this study was to investigate the role of lipoxin A(4), an anti-inflammatory and proresolution mod

66 ivo and in vitro and that spinal delivery of lipoxin A(4), as well as stable analogues, attenuates in

67 oresolution mediators annexin A1 (AnxA1) and lipoxin A(4), as well as the activating and proinflammat

68 l biosynthesis of lipid mediators, including lipoxin A(4), resolvin D1, and protectin D1.

69 hat aspirin triggers the synthesis of 15-epi-lipoxin A(4), which increases NO synthesis through eNOS

70 oxin A(4) methyl ester, an aspirin-triggered lipoxin A(4)-stable analog (ATLa), on the protein phosph

71 e ability to trigger the synthesis of 15-epi-lipoxin A(4).

72 miR-181b overexpression blunted lipoxin A4 (0.1-10 nm)- and resolvin D1 (0.01-10 nm)-sti

73 The proresolving lipid mediator, 15-epi lipoxin A4 (15-epi LXA4), plays a critical role in limit

74 ure coinciding with reduced levels of 15-epi-Lipoxin A4 (15-epi LXA4).

75 peptide (AnxA1Ac2-26) and aspirin-triggered lipoxin A4 (15-epi-lipoxin A4), on the cerebral microcir

76 15-Epi-lipoxin A4 (15-epi-LXA4) blocked agonist-initiated assoc

77 ival crevicular fluid (GCF) levels of 15-epi-lipoxin A4 (15-epi-LXA4), lipoxin A4, leukotriene B4 (LT

78 AWFIENEEQEYVQTVK), 2.5 mug/kg] and 15-epimer-lipoxin A4 (15-epi-LXA4; FPR2/ALX specific, 12.5 and 100

79 r2/3, an ortholog of human FPR2/receptor for lipoxin A4 (ALX), in orchestrating intestinal mucosal re

80 We measured lipoxin A4 (LXA4) and leukotriene B4 (LTB4) levels in EB

81 d levels of the proresolving lipid mediators lipoxin A4 (LXA4) and, in the presence of aspirin, 15-ep

82 Here, lipoxin A4 (LXA4) attenuated TGF-beta1-induced expressio

83 We previously showed that lipoxin A4 (LXA4) controls migration of dendritic cells

84 Cox2 MKO also reduced inflammation resolving lipoxin A4 (LXA4) in intestinal tissue, while administra

85 Also, levels of prostaglandin D2 (PGD2) and lipoxin A4 (LXA4) in patients with T1R were significantl

86 Lipoxin A4 (LXA4) is a potent endogenous lipoxygenase-de

87 Lipoxin A4 (LXA4) is an anti-inflammatory lipid, importa

88 Lipoxin A4 (LXA4) is an endogenous lipid mediator with c

89 Lipoxin A4 (LXA4) is an endogenous lipid mediator with p

90 Lipoxin A4 (LXA4) signaling blocks asthmatic responses i

91 Here we investigated the ability of lipoxin A4 (LXA4) stable analogs to regulate airway resp

92 endogenous agonists for Fpr2/3 revealed that lipoxin A4 (LXA4) was generated by platelet/neutrophil a

93 High levels of lipoxin A4 (LXA4) were detected in sera from infected WT

94 y-old mice were treated with NPD1, PEDF+DHA, lipoxin A4 (LXA4), 12- or 15-hydroxyeicosatetraenoic aci

95 In this study, we investigated whether lipoxin A4 (LXA4), a specialized, proresolution lipid me

96 Lipoxin A4 (LXA4), an endogenous lipoxygenase-derived ei

97 Pro-resolution mediators, such as lipoxin A4 (LXA4), are produced during inflammation retu

98 cosanoids, such as leukotriene B4 (LTB4) and lipoxin A4 (LXA4), may play a key role during obesity.

99 could favor the biosynthesis of proresolving lipoxin A4 (LXA4).

100 nflammatory and proresolving lipid mediator, lipoxin A4 (LXA4).

101 fects of a specialized proresolving mediator lipoxin A4 (LXA4).

102 miting cell for generating anti-inflammatory lipoxin A4 (LXA4).

103 However, lipoxin A4 (LXA4, 0.02-2 microM, a lipid mediator with h

104 ric lipoxins, termed 15-epi-lipoxins (15-epi-lipoxin A4 [e-LXA4]).

105 Moreover, aspirin-triggered lipoxin A4 activation of neutrophil Fpr2/3 regulated neu

106 of two ALX agonists (W peptide and a stable lipoxin A4 analog) exerted cardioprotection in wild-type

107 as rescued by RvE1, PD1 or aspirin-triggered lipoxin A4 analogue.

108 We have also explored other lipid mediators [lipoxin A4 and 15(S)- and 12(S)-hydroxyeicosatetraenoic

109 tor), conveys the proresolving properties of lipoxin A4 and annexin A1 (AnxA1) and the proinflammator

110 allosteric effects of the endogenous ligands lipoxin A4 and pregnenolone at CB1Rs.

111 , C16:1, and C18:1 fatty acids; increases in lipoxin A4 and prostaglandin J2; and a decrease in 20-hy

112 receptor 2 (ALX/FPR2) by the lipid mediators lipoxin A4 and resolvin D1 (RvD1) promotes resolution of

113 Lipoxin A4 augments host defense in sepsis and reduces P

114 ower levels of LTB4 and increased amounts of lipoxin A4 compared with nontransgenic littermates.

115 In contrast, 15-epi-lipoxin A4 did not significantly improve the severity of

116 Pregnenolone but not lipoxin A4 displaced [(3)H]SR141716A, but there was no f

117 lates the secretion of the anti-inflammatory lipoxin A4 in host cells and the viral factors involved

118 reatment, aspirin triggers detectable 15-epi-lipoxin A4 in lung tissue, but not in plasma.

119 In activated whole blood, mean lipoxin A4 levels were decreased in severe compared with

120 We also examined the effect of lipoxin A4 on PP5 activation by IL-2 plus IL-4.

121 n (ATL; 15-epi-lipoxin A4), and blocking the lipoxin A4 receptor (ALX) with a peptide antagonist (Boc

122 e with myeloid-selective expression of human lipoxin A4 receptor (hALX) was prepared and used to eval

123 he AnxA1 receptor (formyl peptide receptor 2/Lipoxin A4 receptor [FPR2/ALX]; IC50 approximately 4 nM)

124 Furthermore, we tested whether the lipoxin A4 receptor formyl-peptide receptor 2/3 (Fpr2/3;

125 The lipoxin A4 receptor FPR2/ALX plays an important part in

126 Fpr2/lipoxin A4 receptor is a therapeutic target for initiati

127 Blocking Fpr2/lipoxin A4 receptor with the antagonist Boc2 reversed th

128 receptor 2/3 (Fpr2/3; ortholog to human FPR2/lipoxin A4 receptor) evoked neuroprotective functions af

129 receptor type 2 (FPR2), also called ALX (the lipoxin A4 receptor), conveys the proresolving propertie

130 rs, including integrins, FPR-like receptor-1/lipoxin A4 receptor, and the epidermal growth factor rec

131 Regulatory mechanisms of ALX/FPR2, the lipoxin A4 receptor, expression have considerable releva

132 vating its receptor formyl peptide receptor2/lipoxin A4 receptor, suppresses cytosolic calcium and de

133 he mRNA for FPR and the structurally related lipoxin A4 receptor, termed ALX; thus, comparable equimo

134 ed microRNA-mediated regulation of ALX/FPR2 (lipoxin A4 receptor/formyl peptide receptor 2) expressio

135 The presence of the lipoxin A4 receptor/formyl peptidyl receptor (ALX/FPR) i

136 inhibition, pretreatment of eosinophils with lipoxin A4 restored GCR phosphorylation and the proaptop

137 treatment with an ALX/FPRL-1 agonist, 15-epi-lipoxin A4 reversed the enhanced sensitivity of AnxA1 (-

138 factor contributing to the downregulation of lipoxin A4 secretion in host cells.

139 enzyme 15-lipoxygenase, which is involved in lipoxin A4 synthesis.

140 The counterregulatory mediator lipoxin A4 was detectable in low picogram amounts, using

141 Basal circulating levels of lipoxin A4 were also decreased in severe relative to mod

142 and 15(S)-hydroxyeicosatetraenoic acid, and lipoxin A4 were found under these conditions.

143 so called ALX because it is the receptor for lipoxin A4) sustains a variety of biological responses r

144 levels of ASA-triggered lipoxin (ATL; 15-epi-lipoxin A4), and blocking the lipoxin A4 receptor (ALX)

145 using an endogenous anti-inflammatory lipid (lipoxin A4), ex vivo in murine aortas, and in vivo via t

146 26) and aspirin-triggered lipoxin A4 (15-epi-lipoxin A4), on the cerebral microcirculation after isch

147 3)--ortholog to human FPR2/ALX (receptor for lipoxin A4)--exerted regulatory and organ-protective fun

148 g cytokine IL-6, which was opposed by 15-epi-lipoxin A4, a counter-regulatory mediator, and ALX/FPR2

149 RM) containing a novel lipoxin analog (benzo-lipoxin A4, bLXA4) to promote regeneration of hard and s

150 r 15-deoxy-Delta(12,14)-prostaglandin-J2 and lipoxin A4, both of which are potent inflammation-resolv

151 eased endogenous levels of aspirin-triggered lipoxin A4, effects again mediated by Fpr2/3.

152 acetyl salicylic acid, acting through 15-epi-lipoxin A4, have been shown to be anti-inflammatory in h

153 ) levels of 15-epi-lipoxin A4 (15-epi-LXA4), lipoxin A4, leukotriene B4 (LTB4), prostaglandin E2 (PGE

154 ces specialized proresolving lipid mediators lipoxin A4, resolvin D1, and resolvin D2 through a RAGE-

155 y 'proresolution' lipid mediators, including lipoxin A4, resolvin E1 and protectin D1.

156 and V) that mediates the release of PAF and lipoxin A4, which, in turn, are responsible for the subs

157 and 3) revealed that PP5 is a target of the lipoxin A4-induced pathway countering cytokine-induced r

158 d to aspirin-triggered lipoxin (ATL), 15-epi-lipoxin A4.

159 arachidonic acid to lipoxins, predominantly Lipoxin A4.

160 ocardial content of lipoxin-A4 and 15(R)-epi-lipoxin-A4 (15-epi-LXA4), both arachidonic acid products

161 one (PIO) increase the myocardial content of lipoxin-A4 and 15(R)-epi-lipoxin-A4 (15-epi-LXA4), both

162 s were harvested and analyzed for myocardial lipoxin-A4 and 15-epi-LXA4 levels and for COX-2 and 5-li

163 n resulted in a small increase in myocardial lipoxin-A4 levels, which was not statistically significa

164 In vitro, 15-epi-lipoxin-A4 reduced the proliferation of LAM patient-deri

165 15-epi-lipoxin-A4 was identified in exhaled breath condensate f

166 rf-2), cyclooxygenase 2 (COX-2) products, or lipoxin action.

167 Here we show that lipoxins activate two receptors in DCs, AhR and LXAR, an

168 esolving medicines (NPRM) containing a novel lipoxin analog (benzo-lipoxin A4, bLXA4) to promote rege

169 umerous reports of the beneficial effects of lipoxin analog administration in animal models of inflam

170 hat administration of a metabolically stable lipoxin analog in a mouse model of the chronic airway in

171 de novo KSHV-infected endothelial cells with lipoxin and epilipoxin creates an anti-inflammatory envi

172 gate whether exhaled breath condensate (EBC) lipoxin and leukotriene measurements can noninvasively c

173 Importantly, receptors for aspirin-triggered lipoxin and resolvin E1 (ALX and ChemR23, respectively)

174 Both aspirin-triggered lipoxin and resolvin E1 block platelet-derived growth fa

175 Lipoxins and aspirin-triggered lipoxins are crucial modu

176 Lipoxins and aspirin-triggered lipoxins are lipid mediat

177 d) in resolving exudates, which also contain lipoxins and aspirin-triggered lipoxins generated from a

178 In addition, aspirin-triggered epi-lipoxins and glucocorticoid-regulated annexin 1 might ac

179 ls: inadequate inflammation caused by excess lipoxins and hyperinflammation driven by excess leukotri

180 The relationship between anti-inflammatory lipoxins and proinflammatory leukotrienes might be impor

181 ated with a "resolution deficit" and whether lipoxins and resolvins influence VSMC phenotype.

182 Recently identified lipid mediators (eg, lipoxins and resolvins) play active roles in promoting t

183 ute inflammation, novel mediators, including lipoxins and resolvins, which are members of the special

184 ated by endogenous lipid agonists, including lipoxins and resolvins.

185 The efficacy of lipoxins and their analog epilipoxins in treating inflam

186 Lipoxins and their aspirin-triggered 15-epimers are endo

187 xygenase pathway generating leukotrienes and lipoxins, and the cytochrome P450 (cP450) pathway produc

188 the arachidonic acid-derived prostaglandins, lipoxins, and their natural C15-epimers.

189 port that plasma levels of aspirin-triggered lipoxin are significantly lower in patients with symptom

190 Lipoxins are anti-inflammatory lipid mediators that modu

191 Lipoxins are biologically active eicosanoids with anti-i

192 Lipoxins and aspirin-triggered lipoxins are crucial modulators of proinflammatory respo

193 It is currently unclear how lipoxins are efficiently formed from precursors or if th

194 Lipoxins are endogenous eicosanoids that demonstrate ant

195 , we provide evidence for a pathway by which lipoxins are generated in macrophages as a consequence o

196 Lipoxins are host anti-inflammatory molecules that play

197 uggests that, while excess anti-inflammatory lipoxins are host detrimental during mycobacterial infec

198 Lipoxins and aspirin-triggered lipoxins are lipid mediators generated from arachidonic

199 Resolvins and lipoxins are lipid mediators generated from essential po

200 Lipoxins are potent anti-inflammatory mediators for neut

201 Lipoxins are potent antiinflammatory lipid mediators tha

202 The use of nature's own molecule lipoxin as a drug is promising.

203 The discovery of lipoxins as a class of endogenous allosteric modulators

204 Here, we establish lipoxins as key chemical mediators in resistance to M. t

205 n and magnitude of inflammation, joining the lipoxins as signals in resolution.

206 -series resolvins, protectins, maresins, and lipoxins at 61 days.

207 can overwhelm organ protective signaling by lipoxins at ALX/FPR2 receptors.

208 as aspirin-triggered resolvins (AT-RvDs) and lipoxins (AT-LXs).

209 E, which is metabolized to aspirin-triggered lipoxin (ATL), 15-epi-lipoxin A4.

210 treatment increased levels of ASA-triggered lipoxin (ATL; 15-epi-lipoxin A4), and blocking the lipox

211 ipid mediators from the prostaglandin to the lipoxin axis.

212 ptotic PMN gave elevated prostaglandin E(2), lipoxin B(4) and RvE2, whereas zymosan-stimulated PMN sh

213 13-series resolvin (RvT)2, RvT4, and 15-epi-lipoxin B(4), compared with those who died.

214 resolvin D3 (AT-RvD3) and aspirin-triggered lipoxin B4 (AT-LXB4).

215 o specialized proresolving mediators (SPMs), lipoxin B4 (LXB4) and resolvin E1 (RvE1), modulate the b

216 he formation of the resolving lipid mediator lipoxin B4, likely by interfering with AA cyclization an

217 associated with hematological functions and lipoxin biogenesis and signaling.

218 n in vivo and suggest that the inhibition of lipoxin biosynthesis could serve as a strategy for enhan

219 This is the first report of a defect in lipoxin biosynthesis in severe asthma, and suggests an a

220 One model of lipoxin biosynthesis involves sequential metabolism of a

221 holipase A2, and its conversion to bioactive lipoxins by 5-lipoxygenase.

222 side of the coin, reporting that endogenous lipoxins compromise immune-mediated control of Mycobacte

223 We report here that lipoxin concentrations in airway fluid were significantl

224 SPMs, which include lipoxins, demonstrate comprehensive protective actions w

225 nsively investigated, LXB4, the less studied lipoxin, emerged to be more potent in protection.

226 also contain lipoxins and aspirin-triggered lipoxins generated from arachidonic acid.

227 Lipoxin generation and its relationship to PGE2 and LTB4

228 ctivity in the cystic fibrosis lung and that lipoxins have therapeutic potential in this lethal autos

229 anti-inflammatory actions of aspirin-induced lipoxins in vivo.

230 harnessing the pleiotropic activities of the lipoxins is a strategy with considerable therapeutic pro

231 riming by inducing the release of a mosquito lipoxin/lipocalin complex.

232 Here we show that this factor consists of a Lipoxin/Lipocalin complex.

233 estigated the potential of aspirin-triggered lipoxin (LX) A4 analog (ATLa), resolving (Rv) D1, and Rv

234 The actions of an aspirin-triggered lipoxin (LX) analog and RvE1 in a human disease, localiz

235 0S, 17S-dihydroxy-docosapentaenoic acid, 15R-Lipoxin (LX)A(4) and n-3 docosapentaenoic-derived Maresi

236 Lipoxins (LX) and their aspirin-triggered 15-epimer endo

237 Lipoxins (LX) are arachidonate-derived pro-resolving med

238 Lipoxins (LX) are bioactive eicosanoids that can be form

239 Lipoxins (LX) are proresolution lipid mediators that inh

240 erated during cell-cell interactions are the lipoxins (LX, including LXA(4) and B(4)), a distinct cla

241 The lipoxins LXA4 and LXB4 are small lipid mediators that ac

242 Lipoxins (Lxs) and aspirin-triggered epi-Lxs (15-epi-LxA

243 Lipoxins (LXs) are eicosanoid mediators that play key co

244 In view of the importance of lipoxins (LXs) in resolving inflammation, we investigate

245 nd II display both beneficial roles, such as lipoxins (LXs) that stereoselectively signal counterregu

246 B(4) and 20-OH-leukotriene B(4), as well as lipoxin marker 5,15-diHETE.

247 o-resolution activity of AT-resolvins and AT-lipoxins may explain some of aspirin's broad anticancer

248 s a pathophysiologically important defect in lipoxin-mediated anti-inflammatory activity in the cysti

249 ts of the immune response, and inhibition of lipoxin-mediated anti-inflammatory responses, which corr

250 s with neutrophils, and we hypothesized that lipoxin mediators regulate formation of neutrophil-plate

251 Together our results demonstrate that lipoxins negatively regulate protective Th1 responses ag

252 iators that include arachidonic acid-derived lipoxins, omega-3 fatty acid eicosapentaenoic acid-deriv

253 lowing acute injury, while inhibition of key lipoxin pathway components exacerbated injury-induced da

254 accumulation of the cyclooxygenase-2-derived lipoxin precursor 15-hydroxyeicosatetraenoic acid (15-HE

255 their ability to convert arachidonic acid to lipoxins, predominantly Lipoxin A4.

256 Thus, epi-lipoxins, produced after aspirin acetylation of inducibl

257 ate leukotriene synthesis but also stimulate lipoxin production in inflammatory cells that do not exp

258 Recent studies implicating deficient lipoxin production in the pathogenesis of diverse inflam

259 ies of lipid mediators, including resolvins, lipoxins, prostaglandins, and leukotrienes, as well as l

260 The antiinflammatory role of peripheral lipoxins raises the hypothesis that similar neuraxial sy

261 multiple approaches were employed using the lipoxin receptor (abbreviated as ALX) dysfunction mouse

262 circuit via formyl peptide receptor (FPR) 2/lipoxin receptor (ALX) (Fpr2/3 in mouse) in global cereb

263 hese effects were partially mediated via the lipoxin receptor (ALX), because they were significantly

264 rial protein release using ELISA, quantified lipoxin receptor (FPR2/ALX) mRNA expression using qRT-PC

265 d airway levels of formyl peptide receptor 2-lipoxin receptor (FPR2/ALXR), LXA4, and its counterregul

266 -7-trihydroxyheptanoic acid methyl ester), a lipoxin receptor agonist, has been previously confirmed

267 gene deletion revealed the importance of the lipoxin receptor ALX for effective lipoxin signaling.

268 at 5-lipoxygenase-dependent (5-LO-dependent) lipoxins regulate host IL-12 production in vivo.

269 This linkage opens the possibility that lipoxins regulate spinal nociceptive processing though t

270 In this regard, lipoxins represent a unique class of lipid mediators tha

271 lammatory leukotrienes and anti-inflammatory lipoxins requires the enzyme 5-lipoxygenase (5-LOX).

272 o-resolving lipid mediators that include the lipoxin, resolvin, protectin and maresin families, colle

273 Given the potent actions of lipoxins, resolvins, and protectins in models of human d

274 y, and proresolving lipid mediators (such as lipoxins, resolvins, and protectins) may suppress proinf

275 cialized proresolving lipid mediators (SPMs; lipoxins, resolvins, and protectins) stimulate resolutio

276 endogenous chemical mediators, for example, lipoxins, resolvins, and protectins.

277 ized proresolving lipid mediators, including lipoxins, resolvins, maresins, and protectins.

278 Specialized pro-resolving mediators (SPM-lipoxins, resolvins, protectins, and maresins) are produ

279 M) constitute separate families that include lipoxins, resolvins, protectins, and maresins, each deri

280 ialized proresolving mediators, specifically lipoxins, resolvins, protectins, and maresins.

281 Among these, lipid mediators, such as the lipoxins, resolvins, protectins, and newly identified ma

282 (SPM) includes essential fatty acid-derived lipoxins, resolvins, protectins, and, most recently, mar

283 research focusing on how the virus modulates lipoxin secretion and warrants further investigation of

284 OX-2-derived mediators, in part via enhanced lipoxin signaling, and carry potential therapeutic impli

285 ce of the lipoxin receptor ALX for effective lipoxin signaling.

286 asthma (SA), display defective generation of lipoxin signals despite glucocorticoid therapy.

287 r arachidonic acid oxygenase activities, the lipoxin synthase activities of 15-lipoxygenating ALOX15

288 evolutionary alterations, we quantified the lipoxin synthase activity of 12-lipoxygenating (rhesus m

289 ssibility that pharmacological inhibition of lipoxin synthesis may provide a method of augmenting ine

290 oduct is transformed via 5-LOX into epimeric lipoxins, termed 15-epi-lipoxins (15-epi-lipoxin A4 [e-L

291 lipid mediators (for example, resolvins and lipoxins) that were modulated by ibuprofen.

292 metabolites while promoting the formation of lipoxins, thus supporting inflammatory resolution.

293 Lipoxin treatment on CRISPR/CAS9 technology-mediated ALX

294 nvestigation of the therapeutic potential of lipoxin using in vitro cell models for KS and PEL.

295 Injection of either lipoxin was sufficient for neuroprotection following acu

296 Lipoxins, which are endogenously produced lipid mediator

297 d-derived prostaglandins and leukotrienes to lipoxins, which initiate the termination sequence.

298 on of anti-inflammatory mediators, including lipoxins, which limit the host inflammatory response and

299 s, as well as arachidonic acid-derived (n-6) lipoxins, which promote resolution of inflammation, clea

300 ries resolvins, protectin D1, maresin 1, and lipoxins) with respect to inflammatory lipid mediators (