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1 ing nature's own anti-inflammatory molecule, lipoxin.
2 uired for synthesis of the anti-inflammatory lipoxins.
3 g eicosanoid substrates to anti-inflammatory lipoxins.
4 rocessing, was attenuated in the presence of lipoxins.
5 in severe asthma include underproduction of lipoxins.
6 valuating the therapeutic potential of using lipoxins.
7 s are classified as aspirin-triggered 15-epi-lipoxins.
8 pacity for antiinflammatory and proresolving lipoxins.
9 ive lipid mediators such as leukotrienes and lipoxins.
10 nals provided by a class of molecules called lipoxins.
11 ors blocked LTC4 and increased resolvins and lipoxins.
12 vel possibility for treating KS and PEL with lipoxins.
13 the production of resolvins, protectins, and lipoxins.
14 resolving mediators, including resolvins and lipoxins.
17 10(5) cells; P < .01), whereas SPM including lipoxin A(4) (977 +/- 173 vs 675 +/- 167 pg/2.5 x 10(5)
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
28 the effect of pro-inflammatory mediators on lipoxin A(4) (LXA(4)) production and FPR2/ALX expression
29 a synthetic nonpsychoactive cannabinoid, and lipoxin A(4) (LXA(4)), an eicosanoid formed from sequent
32 s 15-lipoxygenase (15-LOX) and receptors for lipoxin A(4) (LXA(4)), which have been implicated in an
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
43 he lipid derivatives resolving D1 and D2 and lipoxin A(4) attenuated HLMC histamine release in a dose
45 emaining; synthesis of the anti-inflammatory lipoxin A(4) from arachidonic acid is also detected.
46 d on ultrastructural analysis, IL-8 release, lipoxin A(4) generation, mucin production, and lipoxygen
47 n wild-type mice but both aspirin and 15-epi-lipoxin A(4) had markedly reduced effects on leukocyte-e
49 ere we show that the anti-inflammatory lipid lipoxin A(4) is an endogenous allosteric enhancer of the
50 the effects of 15-epi-16-(p-fluoro)-phenoxy-lipoxin A(4) methyl ester, an aspirin-triggered lipoxin
51 at are both generated in vivo and act at the lipoxin A(4) receptor (ALXR/FPRL1) to halt PMN diapedesi
54 ceptors for RvD1 gave two candidates--ALX, a lipoxin A(4) receptor, and GPR32, an orphan--that were c
56 nistrations of a synthetic aspirin-triggered lipoxin A(4) signal mimetic, ATLa, to probe dynamics of
58 ased more IL-8, and produced lower levels of lipoxin A(4) than that from patients with mild asthma.
63 of this study was to investigate the role of lipoxin A(4), an anti-inflammatory and proresolution mod
64 ivo and in vitro and that spinal delivery of lipoxin A(4), as well as stable analogues, attenuates in
65 oresolution mediators annexin A1 (AnxA1) and lipoxin A(4), as well as the activating and proinflammat
67 nclude the chemotactic peptide fMet-Leu-Phe, lipoxin A(4), serum amyloid A and beta-amyloid peptides.
68 hat aspirin triggers the synthesis of 15-epi-lipoxin A(4), which increases NO synthesis through eNOS
69 oxin A(4) methyl ester, an aspirin-triggered lipoxin A(4)-stable analog (ATLa), on the protein phosph
75 peptide (AnxA1Ac2-26) and aspirin-triggered lipoxin A4 (15-epi-lipoxin A4), on the cerebral microcir
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
81 d levels of the proresolving lipid mediators lipoxin A4 (LXA4) and, in the presence of aspirin, 15-ep
84 Also, levels of prostaglandin D2 (PGD2) and lipoxin A4 (LXA4) in patients with T1R were significantl
90 endogenous agonists for Fpr2/3 revealed that lipoxin A4 (LXA4) was generated by platelet/neutrophil a
93 y-old mice were treated with NPD1, PEDF+DHA, lipoxin A4 (LXA4), 12- or 15-hydroxyeicosatetraenoic aci
97 cosanoids, such as leukotriene B4 (LTB4) and lipoxin A4 (LXA4), may play a key role during obesity.
105 alog of ATL, 15-epi-16-(para-fluoro)-phenoxy-lipoxin A4 analog (ATLa), inhibits neutrophil recruitmen
106 of two ALX agonists (W peptide and a stable lipoxin A4 analog) exerted cardioprotection in wild-type
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
111 receptor 2 (ALX/FPR2) by the lipid mediators lipoxin A4 and resolvin D1 (RvD1) promotes resolution of
113 ower levels of LTB4 and increased amounts of lipoxin A4 compared with nontransgenic littermates.
116 lates the secretion of the anti-inflammatory lipoxin A4 in host cells and the viral factors involved
120 n (ATL; 15-epi-lipoxin A4), and blocking the lipoxin A4 receptor (ALX) with a peptide antagonist (Boc
121 e with myeloid-selective expression of human lipoxin A4 receptor (hALX) was prepared and used to eval
122 he AnxA1 receptor (formyl peptide receptor 2/Lipoxin A4 receptor [FPR2/ALX]; IC50 approximately 4 nM)
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
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
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 (-
139 suboptimal doses (10 ng/mouse) of the ligand lipoxin A4 stable analog compared with <10% reduction of
144 so called ALX because it is the receptor for lipoxin A4) sustains a variety of biological responses r
145 levels of ASA-triggered lipoxin (ATL; 15-epi-lipoxin A4), and blocking the lipoxin A4 receptor (ALX)
146 using an endogenous anti-inflammatory lipid (lipoxin A4), ex vivo in murine aortas, and in vivo via t
147 26) and aspirin-triggered lipoxin A4 (15-epi-lipoxin A4), on the cerebral microcirculation after isch
148 3)--ortholog to human FPR2/ALX (receptor for lipoxin A4)--exerted regulatory and organ-protective fun
149 g cytokine IL-6, which was opposed by 15-epi-lipoxin A4, a counter-regulatory mediator, and ALX/FPR2
150 d mediator that mimics the actions of native lipoxin A4, a putative "stop signal" involved in regulat
151 RM) containing a novel lipoxin analog (benzo-lipoxin A4, bLXA4) to promote regeneration of hard and s
152 r 15-deoxy-Delta(12,14)-prostaglandin-J2 and lipoxin A4, both of which are potent inflammation-resolv
154 acetyl salicylic acid, acting through 15-epi-lipoxin A4, have been shown to be anti-inflammatory in h
155 ) levels of 15-epi-lipoxin A4 (15-epi-LXA4), lipoxin A4, leukotriene B4 (LTB4), prostaglandin E2 (PGE
158 and V) that mediates the release of PAF and lipoxin A4, which, in turn, are responsible for the subs
159 and 3) revealed that PP5 is a target of the lipoxin A4-induced pathway countering cytokine-induced r
163 ocardial content of lipoxin-A4 and 15(R)-epi-lipoxin-A4 (15-epi-LXA4), both arachidonic acid products
164 one (PIO) increase the myocardial content of lipoxin-A4 and 15(R)-epi-lipoxin-A4 (15-epi-LXA4), both
165 s were harvested and analyzed for myocardial lipoxin-A4 and 15-epi-LXA4 levels and for COX-2 and 5-li
166 n resulted in a small increase in myocardial lipoxin-A4 levels, which was not statistically significa
171 esolving medicines (NPRM) containing a novel lipoxin analog (benzo-lipoxin A4, bLXA4) to promote rege
172 umerous reports of the beneficial effects of lipoxin analog administration in animal models of inflam
173 hat administration of a metabolically stable lipoxin analog in a mouse model of the chronic airway in
174 de novo KSHV-infected endothelial cells with lipoxin and epilipoxin creates an anti-inflammatory envi
175 gate whether exhaled breath condensate (EBC) lipoxin and leukotriene measurements can noninvasively c
177 Importantly, receptors for aspirin-triggered lipoxin and resolvin E1 (ALX and ChemR23, respectively)
181 d) in resolving exudates, which also contain lipoxins and aspirin-triggered lipoxins generated from a
183 ls: inadequate inflammation caused by excess lipoxins and hyperinflammation driven by excess leukotri
184 The relationship between anti-inflammatory lipoxins and proinflammatory leukotrienes might be impor
186 Recently identified lipid mediators (eg, lipoxins and resolvins) play active roles in promoting t
187 ute inflammation, novel mediators, including lipoxins and resolvins, which are members of the special
191 xygenase pathway generating leukotrienes and lipoxins, and the cytochrome P450 (cP450) pathway produc
193 port that plasma levels of aspirin-triggered lipoxin are significantly lower in patients with symptom
199 , we provide evidence for a pathway by which lipoxins are generated in macrophages as a consequence o
201 uggests that, while excess anti-inflammatory lipoxins are host detrimental during mycobacterial infec
212 treatment increased levels of ASA-triggered lipoxin (ATL; 15-epi-lipoxin A4), and blocking the lipox
213 EX is a property shared by aspirin-triggered lipoxins (ATL) and the glucocorticoid-induced annexin 1
214 pimers of LXA(4), known as aspirin-triggered lipoxins (ATL), that may account for some of the bioacti
216 ptotic PMN gave elevated prostaglandin E(2), lipoxin B(4) and RvE2, whereas zymosan-stimulated PMN sh
218 he formation of the resolving lipid mediator lipoxin B4, likely by interfering with AA cyclization an
220 n in vivo and suggest that the inhibition of lipoxin biosynthesis could serve as a strategy for enhan
221 This is the first report of a defect in lipoxin biosynthesis in severe asthma, and suggests an a
224 side of the coin, reporting that endogenous lipoxins compromise immune-mediated control of Mycobacte
229 ctivity in the cystic fibrosis lung and that lipoxins have therapeutic potential in this lethal autos
232 harnessing the pleiotropic activities of the lipoxins is a strategy with considerable therapeutic pro
235 estigated the potential of aspirin-triggered lipoxin (LX) A4 analog (ATLa), resolving (Rv) D1, and Rv
242 erated during cell-cell interactions are the lipoxins (LX, including LXA(4) and B(4)), a distinct cla
248 nd II display both beneficial roles, such as lipoxins (LXs) that stereoselectively signal counterregu
250 s a pathophysiologically important defect in lipoxin-mediated anti-inflammatory activity in the cysti
251 ts of the immune response, and inhibition of lipoxin-mediated anti-inflammatory responses, which corr
252 s with neutrophils, and we hypothesized that lipoxin mediators regulate formation of neutrophil-plate
254 iators that include arachidonic acid-derived lipoxins, omega-3 fatty acid eicosapentaenoic acid-deriv
255 lowing acute injury, while inhibition of key lipoxin pathway components exacerbated injury-induced da
256 accumulation of the cyclooxygenase-2-derived lipoxin precursor 15-hydroxyeicosatetraenoic acid (15-HE
259 ate leukotriene synthesis but also stimulate lipoxin production in inflammatory cells that do not exp
261 ies of lipid mediators, including resolvins, lipoxins, prostaglandins, and leukotrienes, as well as l
262 olizing arachidonic acid derivatives such as lipoxins, prostaglandins, hydroxyeicosatetraenoic acids
263 The antiinflammatory role of peripheral lipoxins raises the hypothesis that similar neuraxial sy
264 circuit via formyl peptide receptor (FPR) 2/lipoxin receptor (ALX) (Fpr2/3 in mouse) in global cereb
265 hese effects were partially mediated via the lipoxin receptor (ALX), because they were significantly
266 rial protein release using ELISA, quantified lipoxin receptor (FPR2/ALX) mRNA expression using qRT-PC
267 d airway levels of formyl peptide receptor 2-lipoxin receptor (FPR2/ALXR), LXA4, and its counterregul
268 -7-trihydroxyheptanoic acid methyl ester), a lipoxin receptor agonist, has been previously confirmed
269 gene deletion revealed the importance of the lipoxin receptor ALX for effective lipoxin signaling.
271 This linkage opens the possibility that lipoxins regulate spinal nociceptive processing though t
273 lammatory leukotrienes and anti-inflammatory lipoxins requires the enzyme 5-lipoxygenase (5-LOX).
274 o-resolving lipid mediators that include the lipoxin, resolvin, protectin and maresin families, colle
276 y, and proresolving lipid mediators (such as lipoxins, resolvins, and protectins) may suppress proinf
277 cialized proresolving lipid mediators (SPMs; lipoxins, resolvins, and protectins) stimulate resolutio
280 M) constitute separate families that include lipoxins, resolvins, protectins, and maresins, each deri
282 Among these, lipid mediators, such as the lipoxins, resolvins, protectins, and newly identified ma
283 (SPM) includes essential fatty acid-derived lipoxins, resolvins, protectins, and, most recently, mar
284 research focusing on how the virus modulates lipoxin secretion and warrants further investigation of
285 OX-2-derived mediators, in part via enhanced lipoxin signaling, and carry potential therapeutic impli
288 r arachidonic acid oxygenase activities, the lipoxin synthase activities of 15-lipoxygenating ALOX15
289 evolutionary alterations, we quantified the lipoxin synthase activity of 12-lipoxygenating (rhesus m
290 ssibility that pharmacological inhibition of lipoxin synthesis may provide a method of augmenting ine
291 oduct is transformed via 5-LOX into epimeric lipoxins, termed 15-epi-lipoxins (15-epi-lipoxin A4 [e-L
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 (
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