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Journal articles on the topic 'Lipoxine A4'

Author: Grafiati

Published: 4 June 2021

Last updated: 18 February 2022

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1

Busija, D. W., W. Armstead, C. W. Leffler, and R. Mirro. "Lipoxins A4 and B4 dilate cerebral arterioles of newborn pigs." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 2 (1989): H468—H471. http://dx.doi.org/10.1152/ajpheart.1989.256.2.h468.

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We determined the effects of lipoxins A4 and B4 on the cerebral microcirculation of neonatal pigs and whether vascular responses were modulated by prostanoids. Pial arteriolar diameters were determined using a closed cranial window and intravital microscopy. Before lipoxin A4 application, arteriolar diameter was 143 +/- 6 microns (means +/- SE). Topical application of lipoxin A4 increased the diameter to 160 +/- 7 microns at 0.1 ng/ml, 167 +/- 7 microns at 1 ng/ml, and 173 +/- 7 microns at 10 ng/ml (n = 9). Before application of lipoxin B4, arteriolar diameter was 146 +/- 7 microns. Topical ap

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Chandrasekharan, Jayashree A., Xiao M. Huang, Alexander C. Hwang, and Neelam Sharma-Walia. "Altering the Anti-inflammatory Lipoxin Microenvironment: a New Insight into Kaposi's Sarcoma-Associated Herpesvirus Pathogenesis." Journal of Virology 90, no. 24 (2016): 11020–31. http://dx.doi.org/10.1128/jvi.01491-16.

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ABSTRACTLipoxins are host anti-inflammatory molecules that play a vital role in restoring tissue homeostasis. The efficacy of lipoxins and their analog epilipoxins in treating inflammation and its associated diseases has been well documented. Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL) are two well-known inflammation related diseases caused by Kaposi's sarcoma-associated herpesvirus (KSHV). Controlling inflammation is one of the strategies adopted to treat KS and PEL, a primary motivation for exploring and evaluating the therapeutic potential of using lipoxins. This study documen

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Tułowiecka, Nikola, Dariusz Kotlęga, Andrzej Bohatyrewicz, and Małgorzata Szczuko. "Could Lipoxins Represent a New Standard in Ischemic Stroke Treatment?" International Journal of Molecular Sciences 22, no. 8 (2021): 4207. http://dx.doi.org/10.3390/ijms22084207.

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Introduction: Cardiovascular diseases including stroke are one of the most common causes of death. Their main cause is atherosclerosis and chronic inflammation in the body. An ischemic stroke may occur as a result of the rupture of unstable atherosclerotic plaque. Cardiovascular diseases are associated with uncontrolled inflammation. The inflammatory reaction produces chemical mediators that stimulate the resolution of inflammation. One of these mediators is lipoxins—pro-resolving mediators that are derived from the omega-6 fatty acid family, promoting inflammation relief and supporting tissue

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Chiron, R., Y. Grumbach, Nga Vuthi Quynh, V. Verriere, and V. Urbach. "116 Influence de l’antibiothérapie sur le taux d’IL-8 et de Lipoxine A4 dans les expectorations des patients atteints de mucoviscidose." Revue des Maladies Respiratoires 23, no. 5 (2006): 573. http://dx.doi.org/10.1016/s0761-8425(06)71944-1.

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Svensson, Camilla I., Michela Zattoni, and Charles N. Serhan. "Lipoxins and aspirin-triggered lipoxin inhibit inflammatory pain processing." Journal of Experimental Medicine 204, no. 2 (2007): 245–52. http://dx.doi.org/10.1084/jem.20061826.

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Inflammatory conditions can lead to debilitating and persistent pain. This hyperalgesia reflects sensitization of peripheral terminals and facilitation of pain signaling at the spinal level. Studies of peripheral systems show that tissue injury triggers not only inflammation but also a well-orchestrated series of events that leads to reversal of the inflammatory state. In this regard, lipoxins represent a unique class of lipid mediators that promote resolution of inflammation. The antiinflammatory role of peripheral lipoxins raises the hypothesis that similar neuraxial systems may also down-re

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Grumbach, Y., N. Vu Thi Quynh, and V. Urbach. "095 Effet de la lipoxine A4 sur l’expression de la zonula-occludens-1 et la formation des jonctions serrées dans l’épithelium bronchique." Revue des Maladies Respiratoires 23, no. 5 (2006): 562. http://dx.doi.org/10.1016/s0761-8425(06)71923-4.

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7

Romano, M., X. S. Chen, Y. Takahashi, S. Yamamoto, C. D. Funk, and C. N. Serhan. "Lipoxin synthase activity of human platelet 12-lipoxygenase." Biochemical Journal 296, no. 1 (1993): 127–33. http://dx.doi.org/10.1042/bj2960127.

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Human platelets and megacaryocytes generate lipoxins from exogenous leukotriene A4 (LTA4). We examined the role of human 12-lipoxygenase (12-LO) in lipoxin generation with recombinant histidine-tagged human platelet enzyme (6His-12-LO), partially purified 12-LO from human platelets (HPL 12-LO) and, for the purposes of direct comparison, permeabilized platelets. Recombinant and HPL 12-LO catalysed the conversion of intact LTA4 into both lipoxin A4 (LXA4) and lipoxin B4 (LXB4). In contrast, only negligible quantities of LXA4 were generated when recombinant 12-LO was incubated with the non-enzymi

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Tarannum, Fouzia, and Mohamed Faizuddin. "Effect of Alox-15 Polymorphism on GCF Levels of Lipoxin-A4 in Chronic Periodontitis: A Preliminary Study." Brazilian Dental Journal 28, no. 2 (2017): 140–47. http://dx.doi.org/10.1590/0103-6440201701094.

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Lipoxins play an important role in periodontal resolution, hence, investigation of genetic polymorphism of lipoxin gene may provide important information on the role of lipoxins in periodontal disease pathogenesis. The aim of this study was to investigate a polymorphism of C-to-T substitution at position c.-292 in ALOX15 (reticulocyte-type 15 lipoxygenase 1) gene in patients with chronic periodontitis and to associate the polymorphism with gingival crevicular fluid (GCF) lipoxin A4 (LXA4) levels. Forty-five chronic periodontitis and 45 periodontally healthy patients were included in this case-

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Yu, Suhui, Jianming Xie, Yukai Xiang та ін. "Downregulation of TNF-α/TNF-R1 Signals by AT-Lipoxin A4 May Be a Significant Mechanism of Attenuation in SAP-Associated Lung Injury". Mediators of Inflammation 2019 (11 квітня 2019): 1–13. http://dx.doi.org/10.1155/2019/9019404.

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Our previous studies verified the potent anti-inflammatory effects against severe acute pancreatitis (SAP) of AT-Lipoxin A4 and their analogues. However, the anti-inflammatory effects of AT-Lipoxin A4 on SAP-associated lung injury are not thoroughly known. We used western blot, polymerase chain reaction (PCR), and immunofluorescence to investigate the downregulation of TNF-α signals in cellular and animal models of SAP-associated lung injury following AT-Lipoxin A4 intervention. In vitro, we found that AT-Lipoxin A4 markedly suppressed protein expression in TNF-α signals in human pulmonary mic

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Katoh, T., K. Takahashi, D. K. DeBoer, C. N. Serhan, and K. F. Badr. "Renal hemodynamic actions of lipoxins in rats: a comparative physiological study." American Journal of Physiology-Renal Physiology 263, no. 3 (1992): F436—F442. http://dx.doi.org/10.1152/ajprenal.1992.263.3.f436.

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Interactions between either the arachidonate 5-lipoxygenase (5-LO) and 15-LO or 5-LO and 12-LO can lead to the formation of lipoxins. Although the functional significance of lipoxygenase products of arachidonic acid has been recognized increasingly in glomerular inflammation, less is known regarding the specific effects of lipoxins on renal hemodynamics. Here, we examine the renal actions of lipoxin (LX) A4, LXB4, and, the recently identified 7-cis-11-trans-LXA4, which were administered into the renal artery of the euvolemic male Munich-Wistar rat. LXA4 caused increases in renal plasma flow (R

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Prescott, David, and Derek M. McKay. "Aspirin-triggered lipoxin enhances macrophage phagocytosis of bacteria while inhibiting inflammatory cytokine production." American Journal of Physiology-Gastrointestinal and Liver Physiology 301, no. 3 (2011): G487—G497. http://dx.doi.org/10.1152/ajpgi.00042.2011.

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The macrophage plays a major role in the induction and resolution phases of inflammation; however, how lipid mediator-derived signals may modulate macrophage function in the resolution of inflammation driven by microbes (e.g., in inflammatory bowel disease) is not well understood. We examined the effects of aspirin-triggered lipoxin (ATL), a stable analog of lipoxin A4, on the antimicrobial responses of human peripheral blood mononuclear cell-derived macrophages and the monocytic THP-1 cell line. Additionally, we assessed the expression and localization of the lipoxin receptor, formyl peptide

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Nascimento-Silva, V., M. A. Arruda, C. Barja-Fidalgo, C. G. Villela, and I. M. Fierro. "Novel lipid mediator aspirin-triggered lipoxin A4 induces heme oxygenase-1 in endothelial cells." American Journal of Physiology-Cell Physiology 289, no. 3 (2005): C557—C563. http://dx.doi.org/10.1152/ajpcell.00045.2005.

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Lipoxins (LX) and aspirin-triggered LX (ATL) are eicosanoids generated during inflammation via transcellular biosynthetic routes that elicit distinct anti-inflammatory and proresolution bioactions, including inhibition of leukocyte-mediated injury, stimulation of macrophage clearance of apoptotic neutrophils, repression of proinflammatory cytokine production, and inhibition of cell proliferation and migration. Recently, it was reported that aspirin induces heme oxygenase-1 (HO-1) expression on endothelial cells (EC) in a COX-independent manner, what confers protection against prooxidant insult

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Shanmugalingam, Renuka, XiaoSuo Wang, Penelope Motum, et al. "The 15-Epilipoxin-A4 Pathway with Prophylactic Aspirin in Preventing Preeclampsia: A Longitudinal Cohort Study." Journal of Clinical Endocrinology & Metabolism 105, no. 12 (2020): e4811-e4822. http://dx.doi.org/10.1210/clinem/dgaa642.

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Abstract Introduction The benefit of aspirin in preventing preeclampsia is increasingly recognized; however, its mechanism of action remains unclear. Nonobstetric studies have described an anti-inflammatory effect of aspirin through the 15-epilipoxin-A4 pathway (aspirin-triggered lipoxin [ATL]). However, the anti-inflammatory mechanism of aspirin in the prevention of preeclampsia remains unknown. Objective/Hypothesis To examine (1) the difference in longitudinal endogenous lipoxin-A4 (En-Lipoxin-A4) concentration in low-risk (LR) and high-risk (HR) pregnancies, and (2) the effect of aspirin on

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14

Simchowitz, L., S. Fiore, and C. N. Serhan. "Carrier-mediated transport of lipoxin A4 in human neutrophils." American Journal of Physiology-Cell Physiology 267, no. 6 (1994): C1525—C1534. http://dx.doi.org/10.1152/ajpcell.1994.267.6.c1525.

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Lipoxins and other eicosanoids display potent and selective biological effects on leukocytes. In this study, we utilized radiolabeled lipoxin A4 ([3H]LXA4) to investigate whether carrier-mediated transport of LXA4 might occur in human neutrophils. At a concentration of 5 nM, uptake of [3H]LXA4, above that due to specific binding to receptors, amounted to approximately 0.6 fmol.10(6) cells-1.min-1. This influx was sensitive to a number of anionic inhibitors, including 3,5-diiodosalicylic acid (K0.5 12 microM), pentachlorophenol (K0.5 25 microM), alpha-cyano-beta-(1-phenylindol-3-yl) acrylic aci

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Wang, Qi, Guang-xiao Xu, Qi-hang Tai, and Yan Wang. "Lipoxin A4 Reduces Ventilator-Induced Lung Injury in Rats with Large-Volume Mechanical Ventilation." Mediators of Inflammation 2020 (November 22, 2020): 1–8. http://dx.doi.org/10.1155/2020/6705985.

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Ventilator-induced lung injury (VILI) is a severe and inevitable complication in patients who require mechanical ventilation (MV) for respiratory support. Lipoxin A4 is an endogenous anti-inflammatory and antioxidant mediator. The present study determined the effects of lipoxin A4 on VILI. Twenty-four rats were randomized to the sham, VILI, and lipoxin A4 (LX4) groups. The rats in the VILI and LX4 groups received large-volume MV for 4 hours to simulate VILI. Capillary permeability was evaluated using the PaO2/FiO2 ratio, lung wet/dry weight ratio, and protein level in the lung. VILI-induced in

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Levy, Bruce D., Sherry Bertram, H. H. Tai, et al. "Agonist-induced lipoxin A4 generation: Detection by a novel lipoxin A4-ELISA." Lipids 28, no. 12 (1993): 1047–53. http://dx.doi.org/10.1007/bf02537069.

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Decker, Yann, Gethin McBean та Catherine Godson. "Lipoxin A4 inhibits IL-1β-induced IL-8 and ICAM-1 expression in 1321N1 human astrocytoma cells". American Journal of Physiology-Cell Physiology 296, № 6 (2009): C1420—C1427. http://dx.doi.org/10.1152/ajpcell.00380.2008.

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There is a growing appreciation that endogenously produced mediators may actively promote the resolution of inflammation. Lipoxins (LX) are a group of recently discovered lipid mediators that have been shown to exert anti-inflammatory and proresolution effects on cells of myeloid and nonmyeloid origin. LXs mediate a number of processes, including regression of pro-inflammatory cytokine production, inhibition of cell proliferation, and stimulation of phagocytosis of apoptotic leukocytes by macrophages. Lipoxin A4 (LXA4) is one of the principal LXs formed by mammalian cells. Recently, a G protei

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18

Romano, Mario, Graziella Luciotti, Sebastiano Gangemi, et al. "Urinary Excretion of Lipoxin A4 and Related Compounds: Development of New Extraction Techniques for Lipoxins." Laboratory Investigation 82, no. 9 (2002): 1253–54. http://dx.doi.org/10.1097/01.lab.0000028823.53486.4a.

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Souza, Marcellus H. L. P., Octavio Menezes de Lima, Stella R. Zamuner, Stefano Fiorucci, and John L. Wallace. "Gastritis increases resistance to aspirin-induced mucosal injury via COX-2-mediated lipoxin synthesis." American Journal of Physiology-Gastrointestinal and Liver Physiology 285, no. 1 (2003): G54—G61. http://dx.doi.org/10.1152/ajpgi.00525.2002.

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Products of cyclooxygenase (COX)-2 contribute to mucosal defense. Acetylation of COX-2 by aspirin has been shown to result in the generation of 15(R)-epi-lipoxin A4, which exerts protective effects in the stomach. In gastritis, it is possible that lipoxin A4 makes a greater contribution to mucosal defense. We tested this hypothesis in the rat, by using the iodoacetamide-induced gastritis model. Iodoacetamide was added to the drinking water for 5 days. Rats were then given aspirin, and the extent of gastric damage was blindly assessed 3 h later. Gastric 15(R)-epi-lipoxin A4 and PGE2 levels were

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Hashimoto, Atsushi, Yousuke Murakami, Hidero Kitasato, Izumi Hayashi, and Hirahito Endo. "Glucocorticoids co-interact with lipoxin A4 via lipoxin A4 receptor (ALX) up-regulation." Biomedicine & Pharmacotherapy 61, no. 1 (2007): 81–85. http://dx.doi.org/10.1016/j.biopha.2006.06.023.

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Paul-Clark, Mark J., Thong van Cao, Niloufar Moradi-Bidhendi, Dianne Cooper, and Derek W. Gilroy. "15-epi-lipoxin A4–mediated Induction of Nitric Oxide Explains How Aspirin Inhibits Acute Inflammation." Journal of Experimental Medicine 200, no. 1 (2004): 69–78. http://dx.doi.org/10.1084/jem.20040566.

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The established model for the mechanism of action of aspirin is the inhibition of prostaglandin synthesis. However, this has never fully explained aspirin's repertoire of antiinflammatory properties. We found in acute pleuritis that aspirin, but not salicylate, indomethacin, or piroxicam, increased plasma nitric oxide (NO), which correlated with a reduction in inflammation. Inhibiting aspirin-elicited NO pharmacologically in this model nullified the antiinflammatory effects of aspirin. Moreover, aspirin was not antiinflammatory in either constitutive (eNOS) or inducible NO synthase (iNOS) knoc

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Dias, Irundika H. K., and Helen R. Griffiths. "Current and Future Directions for Targeting Lipoxin A4 in Alzheimer’s Disease." Journal of Alzheimer's Disease 81, no. 1 (2021): 87–90. http://dx.doi.org/10.3233/jad-210121.

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Neuroinflammation has been implicated in Alzheimer’s disease onset and progression. Chronic neuroinflammation is initiated by amyloid-β-activated microglial cells that secrete immuno-modulatory molecules within the brain and into the vasculature. Inflammation is normally self-limiting and actively resolves by “switching off” the generation of pro-inflammatory mediators and by non-phlogistic clearance of spent cells and their debris to restore tissue homeostasis. Deficits in these anti-inflammatory/pro-resolution pathways may predispose to the development of chronic inflammation. The synthesis

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Fischer, Carrie D., Stephanie C. Duquette, Bernard S. Renaux, et al. "Tulathromycin Exerts Proresolving Effects in Bovine Neutrophils by Inhibiting Phospholipases and Altering Leukotriene B4, Prostaglandin E2, and Lipoxin A4Production." Antimicrobial Agents and Chemotherapy 58, no. 8 (2014): 4298–307. http://dx.doi.org/10.1128/aac.02813-14.

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ABSTRACTThe accumulation of neutrophils and proinflammatory mediators, such as leukotriene B4(LTB4), is a classic marker of inflammatory disease. The clearance of apoptotic neutrophils, inhibition of proinflammatory signaling, and production of proresolving lipids (including lipoxins, such as lipoxin A4[LXA4]) are imperative for resolving inflammation. Tulathromycin (TUL), a macrolide used to treat bovine respiratory disease, confers immunomodulatory benefits via mechanisms that remain unclear. We recently reported the anti-inflammatory properties of TUL in bovine phagocytesin vitroand inMannh

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Wu, B., J. A. Walker, D. Temmermand, et al. "Lipoxin A4 promotes more complete inflammation resolution in sepsis compared to stable lipoxin A4 analog." Prostaglandins, Leukotrienes and Essential Fatty Acids 89, no. 1 (2013): 47–53. http://dx.doi.org/10.1016/j.plefa.2013.04.005.

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Maddox, J. F., and C. N. Serhan. "Lipoxin A4 and B4 are potent stimuli for human monocyte migration and adhesion: selective inactivation by dehydrogenation and reduction." Journal of Experimental Medicine 183, no. 1 (1996): 137–46. http://dx.doi.org/10.1084/jem.183.1.137.

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Monocyte recruitment and adherence are important events in inflammatory and vascular diseases. Here, we evaluated the actions of lipoxin A4 (LXA4) and LXB4, a series of lipoxygenase products from arachidonic acid generated by cell-cell interactions, on human monocytes. LXA4 and LXB4 (10(-7) M) each increased monocyte migration in chamber chemotaxis assays and, in migration under agarose, exhibited chemotactic indices similar to those of the chemotactic peptide formyl-methionyl-leucyl-phenylalanine at 10(-10)-10(-8) M and to the chemokine macrophage inflammatory protein-1 alpha (MIP-1 alpha) at

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Hachicha, Mohamed, Marc Pouliot, Nicos A. Petasis та Charles N. Serhan. "Lipoxin (LX)A4 and Aspirin-triggered 15-epi-LXA4 Inhibit Tumor Necrosis Factor 1α–initiated Neutrophil Responses and Trafficking: Regulators of a Cytokine–Chemokine Axis". Journal of Experimental Medicine 189, № 12 (1999): 1923–30. http://dx.doi.org/10.1084/jem.189.12.1923.

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The impact of lipoxin A4 (LXA4) and aspirin-triggered lipoxins (ATLs) was investigated in tumor necrosis factor (TNF)-α–initiated neutrophil (polymorphonuclear leukocyte) responses in vitro and in vivo using metabolically stable LX analogues. At concentrations as low as 1–10 nM, the LXA4 and ATL analogues each inhibited TNF-α–stimulated superoxide anion generation and IL-1β release by human polymorphonuclear leukocytes. These LXA4-ATL actions were time and concentration dependent and proved selective for TNF-α, as these responses were not altered with either GM-CSF– or zymosan-stimulated cells

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Balode, Līga, Gunta Strazda, Normunds Jurka, et al. "Lipoxygenase-Derived Arachidonic Acid Metabolites in Chronic Obstructive Pulmonary Disease." Medicina 48, no. 6 (2011): 43. http://dx.doi.org/10.3390/medicina48060043.

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Background and Objective. Chronic obstructive pulmonary disease (COPD) is characterized by a persistence of inflammation in large and small airways. We hypothesized that this could be caused by the inability of an inflammatory process to resolve. In the resolution of inflammation, a switching of arachidonic acid metabolism from the production of proinflammatory leukotriene B4 (LtB4) to the synthesis of anti-inflammatory lipoxins plays an important role. The aim of our study was to determine the content of lipoxin A4 (LXA4) and LtB4 in induced sputum of patients with exacerbated COPD and to com

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Wenzel, Alexander, and Ger Van Zandbergen. "Lipoxin A4 receptor dependent leishmania infection." Autoimmunity 42, no. 4 (2009): 331–33. http://dx.doi.org/10.1080/08916930902828239.

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Barja-Fidalgo, Christina, Vany Nascimento-Silva, Maria Arruda, and Iolanda Fierro. "Aspirin-triggered lipoxin A4 blocks reactive oxygen species generation in endothelial cells: A novel antioxidative mechanism." Thrombosis and Haemostasis 97, no. 01 (2007): 88–98. http://dx.doi.org/10.1160/th06-06-0315.

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SummaryLipoxins and their aspirin-triggered carbon-15 epimers have emerged as mediators of key events in endogenous anti-inflammation and resolution. However, the implication of these novel lipid mediators on cardiovascular diseases such as hypertension, atherosclerosis, and heart failure has not been investigated. One of the major features shared by these pathological conditions is the increased production of reactive oxygen species (ROS) generated by vascular NAD(P)H oxidase activation. In this study, we have examined whether an aspirin-triggered lipoxin A4 analog (ATL-1) modulates ROS gener

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Rodrı́guez, A., M. Nomen, B. W. Spur, J. J. Godfroid, and T. H. Lee. "Total synthesis of lipoxin A4 and lipoxin B4 from butadiene." Tetrahedron Letters 41, no. 6 (2000): 823–26. http://dx.doi.org/10.1016/s0040-4039(99)02201-7.

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Titos, Esther, Nan Chiang, Charles N. Serhan, et al. "Hepatocytes are a rich source of novel aspirin-triggered 15-epi-lipoxin A4." American Journal of Physiology-Cell Physiology 277, no. 5 (1999): C870—C877. http://dx.doi.org/10.1152/ajpcell.1999.277.5.c870.

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Novel aspirin (ASA)-triggered 15-epi-lipoxins (ATL) comprise new potent bioactive eicosanoids that may contribute to the therapeutic effect of this drug. ATL biosynthesis is initiated by ASA acetylation of cyclooxygenase (COX)-2 and was originally identified during the interaction of leukocytes with either endothelial or epithelial cells. Here, we examined ATL biosynthesis in rat hepatocytes either alone or in coincubation with nonparenchymal liver cells (NPC) and in liver homogenates from ASA-treated rats. Rat hepatocytes and CC-1 cells, a rat hepatocyte cell line, displayed COX-1 but not COX

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Mitchell, S., K. Harvey, C. Godson, and H. R. Brady. "Lipoxin A4-stimulated phagocytosis of apoptotic neutrophils (PMN) by macrophages: A novel anti-inflammatory bioaction of the lipoxins." Prostaglandins & Other Lipid Mediators 59, no. 1-6 (1999): 25. http://dx.doi.org/10.1016/s0090-6980(99)90260-5.

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Chiang, Nan, Iolanda M. Fierro, Karsten Gronert, and Charles N. Serhan. "Activation of Lipoxin a4 Receptors by Aspirin-Triggered Lipoxins and Select Peptides Evokes Ligand-Specific Responses in Inflammation." Journal of Experimental Medicine 191, no. 7 (2000): 1197–208. http://dx.doi.org/10.1084/jem.191.7.1197.

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Lipoxin (LX) A4 and aspirin-triggered LX (ATL) are endogenous lipids that regulate leukocyte trafficking via specific LXA4 receptors (ALXRs) and mediate antiinflammation and resolution. ATL analogues dramatically inhibited human neutrophil (polymorphonuclear leukocyte [PMN]) responses evoked by a potent necrotactic peptide derived from mitochondria as well as a rogue synthetic chemotactic peptide. These bioactive lipid analogues and small peptides each selectively competed for specific 3H-LXA4 binding with recombinant human ALXR, and its N-glycosylation proved essential for peptide but not LXA

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Macdonald, Linsay J., Sheila C. Boddy, Fiona C. Denison, Kurt J. Sales, and Henry N. Jabbour. "A role for lipoxin A4 as an anti-inflammatory mediator in the human endometrium." REPRODUCTION 142, no. 2 (2011): 345–52. http://dx.doi.org/10.1530/rep-11-0021.

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Lipoxin A4is a lipid mediator that elicits anti-inflammatory and pro-resolution actions via its receptor, formyl peptide receptor 2 (FPR2/ALX). In this study, we aimed to investigate the expression and potential role of lipoxin A4and FPR2/ALX in the regulation of inflammation associated with cyclical remodeling of the human endometrium across the menstrual cycle and during early pregnancy. Using quantitative RT-PCR analysis, we found that FPR2/ALX expression is upregulated during the menstrual phase of the cycle and in decidua tissue from the first trimester of pregnancy. We localized the site

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Brancaleone, Vincenzo, Thomas Gobbetti, Nicolas Cenac, et al. "A vasculo-protective circuit centered on lipoxin A4 and aspirin-triggered 15-epi-lipoxin A4 operative in murine microcirculation." Blood 122, no. 4 (2013): 608–17. http://dx.doi.org/10.1182/blood-2013-04-496661.

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Key Points Fpr2/3 activation controls platelet/neutrophil aggregates to afford LXA4 synthesis, thus inhibiting vascular inflammation on reperfusion. Aspirin can jumpstart this circuit by triggering 15-epi-lipoxin synthesis.

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Kong, Xia, Sheng-Hua Wu, Li Zhang, and Xiao-Qing Chen. "Pilot application of lipoxin A4 analog and lipoxin A4 receptor agonist in asthmatic children with acute episodes." Experimental and Therapeutic Medicine 14, no. 3 (2017): 2284–90. http://dx.doi.org/10.3892/etm.2017.4787.

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Fiore, Stefano, and Charles N. Serhan. "Lipoxin A4 Receptor Activation Is Distinct from That of the Formyl Peptide Receptor in Myeloid Cells: Inhibition of CD11/18 Expression by Lipoxin A4-Lipoxin A4 Receptor Interaction." Biochemistry 34, no. 51 (1995): 16678–86. http://dx.doi.org/10.1021/bi00051a016.

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Lee, Tak H., Claire E. Horton, U. Kyan-Aung, Dorian Haskard, Atttlio E. G. Crea, and Bernd W. Spur. "Lipoxin A4 and Lipoxin B4 Inhibit Chemotactic Responses of Human Neutrophils Stimulated by Leukotriene B4 and N-Formyl-l-Methionyl-l-Leucyl-l-Phenylalanine." Clinical Science 77, no. 2 (1989): 195–203. http://dx.doi.org/10.1042/cs0770195.

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1. Lipoxin A4 (LXA4) and lipoxin B4 (LXB4) have been evaluated for their capacities to modulate neutrophil (PMN) migration and endothelial cell adherence using compounds prepared by total chemical synthesis. 2. Increased PMN migration was seen with concentrations of LXA4 from 10−9 mol/l to 10−7 mol/l. LXA4 was 100-fold less potent than leukotriene B4 (LTB4) and it elicited only one-half of the maximal response of LTB4. 3. The (5S,6S,15S)-isomer of LXA4 induced only a weak migratory response and LXB4 was inactive, suggesting that the activity of LXA4 was stereospecific. 4. Modified chequerboard

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Lee, T. H. "Lipoxin A4: a novel anti-inflammatory molecule?" Thorax 50, no. 2 (1995): 111–12. http://dx.doi.org/10.1136/thx.50.2.111.

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Maderna, Paola, Catherine Godson, Gary Hannify, Madeline Murphy, and Hugh R. Brady. "Influence of lipoxin A4 and other lipoxygenase-derived eicosanoids on tissue factor expression." American Journal of Physiology-Cell Physiology 279, no. 4 (2000): C945—C953. http://dx.doi.org/10.1152/ajpcell.2000.279.4.c945.

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Lipoxins (LX) are eicosanoids generated via transcellular biosynthetic routes during inflammation, hypersensitivity reaction, and after angioplasty. LXs are modulators of leukocyte trafficking and vascular tone. Their influence on the coagulation cascade has not been determined. In this study, we evaluated the influence of LXs on the expression of tissue factor (TF), a key regulator of coagulation. TF activity was measured in lysates of monocytes, human umbilical vein endothelial cells, and ECV304 cells using a one-stage clotting assay. LXA4 stimulated TF activity in each cell type. The influe

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Fierro, Iolanda M., Jeffery L. Kutok, and Charles N. Serhan. "Novel Lipid Mediator Regulators of Endothelial Cell Proliferation and Migration: Aspirin-Triggered-15R-Lipoxin A4 and Lipoxin A4." Journal of Pharmacology and Experimental Therapeutics 300, no. 2 (2002): 385–92. http://dx.doi.org/10.1124/jpet.300.2.385.

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Gronert, Karsten, Andrew Gewirtz, James L. Madara та Charles N. Serhan. "Identification of a Human Enterocyte Lipoxin A4 Receptor That Is Regulated by Interleukin (IL)-13 and Interferon γ and Inhibits Tumor Necrosis Factor α–induced IL-8 Release". Journal of Experimental Medicine 187, № 8 (1998): 1285–94. http://dx.doi.org/10.1084/jem.187.8.1285.

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Epithelial cells of the alimentary tract play a central role in mucosal immunophysiology. Pathogens and/or agonists that interact with mucosal surfaces often elicit epithelial responses that upregulate inflammation. Therefore, it was of interest to explore potential epithelial targeted antiinflammatory signals. Here we identified and sequenced a human enterocyte lipoxin (LX) A4 [5(S),6(R),15(S)-trihydroxy-7,9,13-trans-11-cis eicosatetraenoic acid] receptor, and demonstrate that transcription of this receptor was controlled by cytokines, of which lymphocyte-derived interleukin (IL)-13 and inter

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Martini, Alessandra Cadete, Stefânia Forner, Allisson Freire Bento, and Giles Alexander Rae. "Neuroprotective Effects of Lipoxin A4 in Central Nervous System Pathologies." BioMed Research International 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/316204.

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Many diseases of the central nervous system are characterized and sometimes worsened by an intense inflammatory response in the affected tissue. It is now accepted that resolution of inflammation is an active process mediated by a group of mediators that can act in synchrony to switch the phenotype of cells, from a proinflammatory one to another that favors the return to homeostasis. This new genus of proresolving mediators includes resolvins, protectins, maresins, and lipoxins, the first to be discovered. In this short review we provide an overview of current knowledge into the cellular and m

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Fiore, S., S. W. Ryeom, P. F. Weller, and C. N. Serhan. "Lipoxin recognition sites. Specific binding of labeled lipoxin A4 with human neutrophils." Journal of Biological Chemistry 267, no. 23 (1992): 16168–76. http://dx.doi.org/10.1016/s0021-9258(18)41982-5.

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Nicolaou, K. C., B. E. Marron, C. A. Veale, S. E. Webber, and C. N. Serhan. "Total synthesis of novel geometric isomers of lipoxin A4 and lipoxin B4." Journal of Organic Chemistry 54, no. 23 (1989): 5527–35. http://dx.doi.org/10.1021/jo00284a026.

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Rodriguez, A., M. Nomen, B. W. Spur, J. J. Godfroid, and T. H. Lee. "ChemInform Abstract: Total Synthesis of Lipoxin A4 and Lipoxin B4 from Butadiene." ChemInform 31, no. 16 (2010): no. http://dx.doi.org/10.1002/chin.200016251.

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Szczuko, Małgorzata, Joanna Palma, Justyna Kikut, Natalia Komorniak, and Maciej Ziętek. "Changes of lipoxin levels during pregnancy and the monthly-cycle, condition the normal course of pregnancy or pathology." Inflammation Research 69, no. 9 (2020): 869–81. http://dx.doi.org/10.1007/s00011-020-01358-6.

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Abstract Objective and Design The purpose of the review was to gather information on the role and possibilities of using lipoxin in the treatment of infertility and maintaining a normal pregnancy. Ovulation, menstruation, embryo implantation, and childbirth are reactions representing short-term inflammatory events involving lipoxin activities. Lipoxin A4 (LXA4) is an arachidonic acid metabolite, and in cooperation with its positional isomer lipoxin B4 (LXB4), it is a major lipoxin in mammals. Biosynthesis process occurs in two stages: in the first step, the donor cell releases the eicosanoid i

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Köhnke, Thomas, Beate Gomolka, Süleyman Bilal, et al. "Acetylsalicylic Acid Reduces the Severity of Dextran Sodium Sulfate-Induced Colitis and Increases the Formation of Anti-Inflammatory Lipid Mediators." BioMed Research International 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/748160.

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The role of non-steroidal anti-inflammatory drugs in inflammatory bowel disease is controversial, as they have been implicated in disease aggravation. Different from other cyclooxygenase inhibitors, acetylsalicylic acid (ASA) enhances the formation of anti-inflammatory and proresolution lipoxins derived from arachidonic acid as well as resolvins from omega-3 polyunsaturated fatty acids such as docosahexaenoic acid (DHA). In this study, we examined the effect of ASA on murine dextran sodium sulfate colitis. A mouse magnetic resonance imaging (MRI) protocol and post mortem assessment were used t

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Han, Xue, Weifeng Yao, Zipeng Liu, et al. "Lipoxin A4 Preconditioning Attenuates Intestinal Ischemia Reperfusion Injury through Keap1/Nrf2 Pathway in a Lipoxin A4 Receptor Independent Manner." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/9303606.

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Oxidative stress plays a critical role in the pathogenesis of intestinal ischemia reperfusion (IIR) injury. Enhancement in endogenous Lipoxin A4 (LXA4), a potent antioxidant and mediator, is associated with attenuation of IIR. However, the effects of LXA4 on IIR injury and the potential mechanisms are unknown. In a rat IIR (ischemia 45 minutes and subsequent reperfusion 6 hours) model, IIR caused intestinal injury, evidenced by increased serum diamine oxidase, D-lactic acid, intestinal-type fatty acid-binding protein, and the oxidative stress marker 15-F2t-Isoprostane. LXA4 treatment significa

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Chinthamani, Sreedevi, Olutayo Odusanwo, Nandini Mondal, Joel Nelson, Sriram Neelamegham, and Olga J. Baker. "Lipoxin A4inhibits immune cell binding to salivary epithelium and vascular endothelium." American Journal of Physiology-Cell Physiology 302, no. 7 (2012): C968—C978. http://dx.doi.org/10.1152/ajpcell.00259.2011.

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Lipoxins are formed by leukocytes during cell-cell interactions with epithelial or endothelial cells. Native lipoxin A4(LXA4) binds to the G protein-coupled lipoxin receptors formyl peptide receptor 2 (FPR2)/ALX and CysLT1. Furthermore, LXA4inhibits recruitment of neutrophils, by attenuating chemotaxis, adhesion, and transmigration across vascular endothelial cells. LXA4thus appears to serve as an endogenous “stop signal” for immune cell-mediated tissue injury (Serhan CN; Annu Rev Immunol 25: 101–137, 2007). The role of LXA4has not been addressed in salivary epithelium, and little is known abo

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