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Journal articles on the topic 'Leukotrienes'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Uotila, P., K. Punnonen, R. Tammivaara, and CT Jansén. "Detection of leukotrienes in the serum of asthmatic and psoriatic patients." Acta Dermato-Venereologica 66, no. 5 (1986): 381–85. http://dx.doi.org/10.2340/0001555566381385.

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Purified serum samples from asthmatic and psoriatic patients and healthy controls were analysed by high-pressure liquid chromatography (HPLC) and the amounts of leukotrienes were measured from the corresponding HPLC fractions by specific radioimmunoassays. In the serum of healthy controls the amounts of leukotrienes B4, C4 and D4 were very small or negligible. Rather great amount of leukotriene B4 was, however, detected in the serum of many asthmatic and psoriatic patients. The amount of leukotriene B4 was in the serum of asthmatic patients 120 +/- 20 pmol/ml (n = 11, mean +/- SEM) and in that

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2

Paterson, N. A. "Influence of hypoxia on histamine and leukotriene release from dispersed porcine lung cells." Journal of Applied Physiology 61, no. 5 (1986): 1790–95. http://dx.doi.org/10.1152/jappl.1986.61.5.1790.

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The ability of hypoxia (PO2 57 Torr) and anoxia (PO2 0 Torr) to induce the release of histamine or sulfidopeptide leukotrienes from dispersed porcine parenchymal lung cells was examined. Spontaneous release of histamine (9.2 +/- 1.3%) was not significantly increased during hypoxia or anoxia, and spontaneous leukotriene release was not detected under any conditions. The release of leukotriene induced by A23187 (78 +/- 11 pmol leukotriene D4 equivalent/10(7) parenchymal lung cells) was unchanged during hypoxia and was significantly reduced (55.4 +/- 7.7% control leukotriene release) during anoxi

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3

Petersen, Bodil, K. Frank Austen, Kenneth D. Bloch, et al. "Cysteinyl Leukotrienes Impair Hypoxic Pulmonary Vasoconstriction in Endotoxemic Mice." Anesthesiology 115, no. 4 (2011): 804–11. http://dx.doi.org/10.1097/aln.0b013e31822e94bd.

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Background Sepsis impairs hypoxic pulmonary vasoconstriction (HPV) in patients and animal models, contributing to systemic hypoxemia. Concentrations of cysteinyl leukotrienes are increased in the bronchoalveolar lavage fluid of patients with sepsis, but the contribution of cysteinyl leukotrienes to the impairment of HPV is unknown. Methods Wild-type mice, mice deficient in leukotriene C(4) synthase, the enzyme responsible for cysteinyl leukotriene synthesis, and mice deficient in cysteinyl leukotriene receptor 1 were studied 18 h after challenge with either saline or endotoxin. HPV was measure

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4

Jackson, W. F. "Regional differences in mechanism of action of oxygen on hamster arterioles." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 2 (1993): H599—H603. http://dx.doi.org/10.1152/ajpheart.1993.265.2.h599.

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Leukotrienes have been implicated in the arteriolar constriction induced by elevated PO2 in the hamster cheek pouch. The role of leukotrienes in arteriolar O2 reactivity in other tissues has not been studied. To test the hypothesis that leukotrienes mediate O2 reactivity in all tissues, the effects of a leukotriene receptor antagonist, SKF-102922 (10 microM), a 5-lipoxygenase inhibitor, SC-43251 (30 microM), and a 5-lipoxygenase-activating protein antagonist, MK-886 (10 microM), on arteriolar O2 reactivity in hamster cheek pouch were compared with their effects on cremasteric arteriolar O2 rea

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5

Denzlinger, C., A. Kapp, M. Grimberg, HH Gerhartz, and W. Wilmanns. "Enhanced endogenous leukotriene biosynthesis in patients treated with granulocyte-macrophage colony-stimulating factor." Blood 76, no. 9 (1990): 1765–70. http://dx.doi.org/10.1182/blood.v76.9.1765.1765.

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Abstract The hematopoietic cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) is being used in clinical trials for its potential in the treatment of hematopoietic insufficiency due to various causes. Involvement of leukotrienes in the effects of GM-CSF is suggested by analytical and pharmacologic evidence obtained in vitro. However, until now no data in support of a role of leukotrienes in GM-CSF action in vivo have been presented. In the present investigation this question was approached by measurement of endogenous cysteinyl leukotriene formation in patients treated with the

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6

Denzlinger, C., A. Kapp, M. Grimberg, HH Gerhartz, and W. Wilmanns. "Enhanced endogenous leukotriene biosynthesis in patients treated with granulocyte-macrophage colony-stimulating factor." Blood 76, no. 9 (1990): 1765–70. http://dx.doi.org/10.1182/blood.v76.9.1765.bloodjournal7691765.

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The hematopoietic cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) is being used in clinical trials for its potential in the treatment of hematopoietic insufficiency due to various causes. Involvement of leukotrienes in the effects of GM-CSF is suggested by analytical and pharmacologic evidence obtained in vitro. However, until now no data in support of a role of leukotrienes in GM-CSF action in vivo have been presented. In the present investigation this question was approached by measurement of endogenous cysteinyl leukotriene formation in patients treated with the cytokine

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7

Jones, T. R., Y. Guindon, R. Young та ін. "L-648,051, sodium 4-[3-(4-acetyl-3-hydroxy-2-propylphenoxy)-propylsulfonyl]-γ-oxo-benzenebutanoate: a leukotriene D4 receptor antagonist". Canadian Journal of Physiology and Pharmacology 64, № 12 (1986): 1535–42. http://dx.doi.org/10.1139/y86-258.

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L-648,051, sodium 4-[3-(4-acetyl-3-hydroxy-2-propylphenoxy)propylsulfonyl]-γ-oxo-benzenebutanoate is a selective and competitive inhibitor of [3H]leukotriene D4 (KB value of 4.0 μM) and to a lesser extent [3H]leukotriene C4 (Ki value of 36.7 μM) binding in guinea pig lung homogenates. Functionally, it selectively antagonized contractions of guinea pig trachea induced by leukotrienes C4, D4, E4, and F4 in concentrations that did not antagonize contractions induced by acetylcholine, histamine, serotonin, prostaglandin F2α, or U-44069 (endoperoxide analogue). Schild plot analysis indicated that L

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8

Mancuso, Peter, Theodore J. Standiford, Teresa Marshall, and Marc Peters-Golden. "5-Lipoxygenase Reaction Products Modulate Alveolar Macrophage Phagocytosis of Klebsiella pneumoniae." Infection and Immunity 66, no. 11 (1998): 5140–46. http://dx.doi.org/10.1128/iai.66.11.5140-5146.1998.

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ABSTRACT The leukotrienes are potent lipid mediators of inflammation formed by the 5-lipoxygenase-catalyzed oxidation of arachidonic acid. Although the effects of leukotrienes on neutrophil chemotaxis and activation have been established, their role in modulating innate host defense mechanisms is poorly understood. In a previous study (M. Bailie, T. Standiford, L. Laichalk, M. Coffey, R. Strieter, and M. Peters-Golden, J. Immunol. 157:5221–5224, 1996), we used 5-lipoxygenase knockout mice to establish a critical role for endogenous leukotrienes in pulmonary clearance and alveolar macrophage ph

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9

Meshram, Deepak, Khushbo Bhardwaj, Charulata Rathod, Gail B. Mahady, and Kapil K. Soni. "The Role of Leukotrienes Inhibitors in the Management of Chronic Inflammatory Diseases." Recent Patents on Inflammation & Allergy Drug Discovery 14, no. 1 (2020): 15–31. http://dx.doi.org/10.2174/1872213x14666200130095040.

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Background: Leukotrienes are powerful mediators of inflammation and interact with specific receptors in target cell membrane to initiate an inflammatory response. Thus, Leukotrienes (LTs) are considered to be potent mediators of inflammatory diseases including allergic rhinitis, inflammatory bowel disease and asthma. Leukotriene B4 and the series of cysteinyl leukotrienes (C4, D4, and E4) are metabolites of arachidonic acid metabolism that cause inflammation. The cysteinyl LTs are known to increase vascular permeability, bronco-constriction and mucus secretion. Objectives: To review the publis

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10

Steinhilber, D. "5-Lipoxygenase: A Target for Antiinflammatory Drugs Revisited." Current Medicinal Chemistry 6, no. 1 (1999): 71–85. http://dx.doi.org/10.2174/0929867306666220207211259.

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Abstract: Arachidonate 5-lipoxygenase is the key enzyme in leukotriene biosynthesis and catalyzes the initial steps in the conversion of arachidonic acid to biologically active leukotrienes. Leukotrienes are considered as potent potent mediators of inflammatory and allergic reactions which are locally released by leukocytes and other 5-LO expressing cells and exert their effects via binding to specific membrane receptors and, as suggested recently, the nuclear receptor PPARa. Because of the proinflammatory profile of leukotrienes it was assumed that leukotriene biosynthesis inhibitors and leuk

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11

Craft, D. V., D. J. Lefer, C. E. Hock, and A. M. Lefer. "Significance of production of peptide leukotrienes in murine traumatic shock." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 1 (1986): H80—H85. http://dx.doi.org/10.1152/ajpheart.1986.251.1.h80.

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We studied the formation of a leukotriene metabolite in plasma and bile during traumatic shock. Anesthetized rats subjected to Noble-Collip drum trauma developed a lethal shock state characterized by a survival time of 1.9 +/- 0.3 h, a 4.5-fold increase in plasma cathepsin D activity, and a reduction in mean arterial blood pressure to 45 +/- 2 mmHg compared with 108 +/- 5 mmHg in sham-shock controls. Plasma and bile samples were analyzed by reverse-phase high-pressure liquid chromatography (HPLC) for peptide leukotrienes (e.g., LTC4, LTD4, and LTE4), and their retention times were confirmed by

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12

Hagmann, W. "Cell proliferation status, cytokine action and protein tyrosine phosphorylation modulate leukotriene biosynthesis in a basophil leukaemia and a mastocytoma cell line." Biochemical Journal 299, no. 2 (1994): 467–72. http://dx.doi.org/10.1042/bj2990467.

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Mast cells, mastocytoma cells and basophil leukaemia cells are well-established producers of leukotrienes when grown and stimulated appropriately. I report that the cells' ability to produce leukotrienes is dependent on the cells' proliferative status or their provision with growth factors. Proliferating MC/9 and subconfluent RBL2H3 cells respond maximally to stimulation by 1 microM ionomycin with the production of 56 and 32 pmol of cysteinyl-leukotrienes/10(6) cells respectively. In contrast, confluent RBL2H3 or growth-arrested MC/9 cells lose their ability to generate leukotrienes in respons

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13

Jaeschke, H., M. J. Raftery, U. Justesen, and S. J. Gaskell. "Serum complement mediates endotoxin-induced cysteinyl leukotriene formation in rats in vivo." American Journal of Physiology-Gastrointestinal and Liver Physiology 263, no. 6 (1992): G947—G952. http://dx.doi.org/10.1152/ajpgi.1992.263.6.g947.

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To investigate potential mediators responsible for cysteinyl leukotriene formation during endotoxemia, male Fischer rats received an intravenous bolus injection of 5 mg/kg Salmonella enteritidis endotoxin and cysteinyl leukotrienes were measured by gas chromatography-mass spectrometry. The biliary excretion of leukotriene (LT) C4 (0.20 +/- 0.02 pmol.min-1.g liver-1) and N-acetyl-LTE4 (0.37 +/- 0.07 pmol.min-1.g-1) was increased by 190 and 1,000%, respectively, during the first 30 min after endotoxin injection. Endotoxin also caused a temporary reduction of hepatic ATP levels by 84%. Depletion

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14

Ochkur, Sergei, Cheryl Protheroe, Wen Li, et al. "Cys-leukotrienes mediate lung dysfunction but not histopathologies in an IL-5/Eotaxin-2 double transgenic mouse model of severe asthma (163.13)." Journal of Immunology 186, no. 1_Supplement (2011): 163.13. http://dx.doi.org/10.4049/jimmunol.186.supp.163.13.

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Abstract Products of the 5-lipoxygenase (5-LO) pathway (i.e., cys-leukotrienes and LTB4), are contributors to lung inflammation, airway remodeling, and hyperresponsiveness associated with allergic respiratory inflammation. Eosinophils are capable of leukotriene synthesis/secretion and chemotactically respond to these compounds. However, the in vivo role of eosinophils in leukotriene mediated events during asthmatic airway inflammation is not defined. To study the link between eosinophils and leukotrienes we used the I5/E2 double transgenic mouse model of severe asthma, over-expressing IL-5 sys

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15

Unterberg, Andreas, Walter Schmidt, Michael Wahl, Earl F. Ellis, Anthony Marmarou, and Alexander Baethmann. "Evidence against leukotrienes as mediators of brain edema." Journal of Neurosurgery 74, no. 5 (1991): 773–80. http://dx.doi.org/10.3171/jns.1991.74.5.0773.

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✓ Leukotrienes are powerful metabolites of arachidonic acid which are known to increase the permeability of peripheral blood vessels. These substances are found in brain tissue in association with cerebral ischemia, and in brain tumors. Therefore, it has been proposed that leukotrienes have a mediator function in brain edema. This hypothesis was subjected to further experimental analysis in this study, in which the authors investigated whether: 1) superfusion of the exposed brain surface with leukotrienes increases the permeability of extraparenchymal blood vessels in vivo; 2) intraparenchymal

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16

Larsen, Julie S., and Edward P. Acosta. "Leukotriene-Receptor Antagonists and 5-Lipoxygenase Inhibitors in Asthma." Annals of Pharmacotherapy 27, no. 7-8 (1993): 898–903. http://dx.doi.org/10.1177/106002809302700718.

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OBJECTIVE: To familiarize readers with a potentially new class of compounds for treating asthma. Background information on leukotrienes is provided in addition to an indepth review of pertinent clinical trials. DATA SOURCES: Information was obtained from controlled clinical trials, abstracts, and review articles identified through a MEDLINE search of English-language articles. STUDY SELECTION: Emphasis was placed on early clinical trials that showed some benefit with these compounds as well as more recent studies using newer agents that produced more promising results. DATA EXTRACTION: Informa

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17

Heller, R. Scott, R. Peter Herman, and Ceil A. Herman. "The action and metabolism of peptide leukotrienes in the isolated bullfrog lung." Canadian Journal of Physiology and Pharmacology 67, no. 4 (1989): 309–14. http://dx.doi.org/10.1139/y89-050.

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Leukotrienes (LTs) have been shown to cause contraction of mammalian airway smooth muscle. In this study, LTC4, LTD4, and LTE4 were tested on isolated strips of bullfrog lung. LTC4, LTD4, and LTE4 (10−7 to 3 × 10−10 M) stimulated lung contraction. LTC4 was the most potent, with LTD4 and LTE4 being of equal but lower potency. The cyclooxygenase inhibitors, indomethacin and ibuprofen, had no effect on the strength of leukotriene-induced contraction. In addition, the effects of three mammalian LTD4 receptor antagonists, L-649,923, L-648,051, and LY171883 were tested. All three antagonists failed

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18

Herman, C. A., G. A. Charlton, and R. L. Cranfill. "Metabolism and cardiovascular effects of leukotrienes in warm- and cold-acclimated American bullfrogs (Rana catesbeiana)." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 260, no. 5 (1991): R834—R838. http://dx.doi.org/10.1152/ajpregu.1991.260.5.r834.

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Sulfidopeptide leukotrienes are important mediators in mammals, but much less is known of their metabolism and action in nonmammalian vertebrates. This study examines the cardiovascular effects of leukotrienes on blood pressure and heart rate and compares the metabolism of leukotrienes in vivo and in vitro in warm- and cold-acclimated bullfrogs. Leukotriene C4 (LTC4) is more potent than leukotriene D4 (LTD4) and leukotriene E4 (LTE4) in eliciting hypotension. The leukotrienes are more potent in warm-acclimated animals. Conversion of [3H]LTC4 to [3H]LTD4 occurs rapidly in warm-acclimated bullfr

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19

Jones, T. R., R. Young, E. Champion та ін. "L-649,923, Sodium (βS*, γR*)-4-(3-(4-acetyl-3-hydroxy-2-propylphenoxy)-propylthio)-γ-hydroxy-β-methylbenzenebutanoate, a selective, orally active leukotriene receptor antagonist". Canadian Journal of Physiology and Pharmacology 64, № 8 (1986): 1068–75. http://dx.doi.org/10.1139/y86-183.

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L-649,923, Sodium (βs*, γR*)-4-(3-(4-acetyi-3-hydroxy-2-propylphenoxy)propylthio)-γ-hydroxy-β-methylbenzenebutanoate is a selective and competitive inhibitor of [3H]leukotriene D4 (Ki value of 400 nM) and to a lesser extent [3H]leukotriene C4 (Ki value of 8.6 μM) binding in guinea-pig lung homogenates. Functionally, it selectively antagonized contractions of guinea pig trachea induced by leukotriene C4, D4, E4, and F4 but not those induced by acetylcholine, histamine, serotonin, prostaglandin F2α, or U-44069 (stable endoperoxide analogue). Schild plot analysis indicated a competitive inhibitio

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Leikauf, G. D., H. E. Claesson, C. A. Doupnik, S. Hybbinette, and R. C. Grafstrom. "Cysteinyl leukotrienes enhance growth of human airway epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 259, no. 4 (1990): L255—L261. http://dx.doi.org/10.1152/ajplung.1990.259.4.l255.

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Epithelial inflammation may play an obligatory role in the pathogenesis of a number of chronic pulmonary diseases such as asthma or bronchitis and has been implicated during the promotion phase of multistage carcinogenesis. At sites of inflammation, bioactive lipid mediators are released and activate a wide range of pathophysiological responses including bronchospasm. Previous studies suggest that one class of inflammatory mediators, the eicosanoids, can also influence cell growth. Epithelial cell proliferation and hyperplasia are common sequelae to irritation and inflammation, and because the

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21

Murphy, Robert C., and Miguel A. Gijón. "Biosynthesis and metabolism of leukotrienes." Biochemical Journal 405, no. 3 (2007): 379–95. http://dx.doi.org/10.1042/bj20070289.

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Leukotrienes are metabolites of arachidonic acid derived from the action of 5-LO (5-lipoxygenase). The immediate product of 5-LO is LTA4 (leukotriene A4), which is enzymatically converted into either LTB4 (leukotriene B4) by LTA4 hydrolase or LTC4 (leukotriene C4) by LTC4 synthase. The regulation of leukotriene production occurs at various levels, including expression of 5-LO, translocation of 5-LO to the perinuclear region and phosphorylation to either enhance or inhibit the activity of 5-LO. Several other proteins, including cPLA2α (cytosolic phospholipase A2α) and FLAP (5-LO-activating prot

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22

Rola-Pleszczynski, Marek, and Jana Stankova. "Cytokine-Leukotriene Receptor Interactions." Scientific World JOURNAL 7 (2007): 1348–58. http://dx.doi.org/10.1100/tsw.2007.183.

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Biochemical and pharmacological studies have identified the structure of leukotrienes, the pathways that lead to their synthesis, and the signaling events they trigger when they interact with their cognate receptors. A privileged interaction exists between these lipid mediators and another group of molecules essential for inflammation and immune modulation, namely, cytokines. Whereas leukotrienes can trigger the synthesis and release of selected cytokines in distinct cell populations, many cytokines can affect cellular responsiveness to leukotrienes by modulating leukotriene receptor expressio

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Denzlinger, C., W. Tetzloff, HH Gerhartz, et al. "Differential activation of the endogenous leukotriene biosynthesis by two different preparations of granulocyte-macrophage colony-stimulating factor in healthy volunteers." Blood 81, no. 8 (1993): 2007–13. http://dx.doi.org/10.1182/blood.v81.8.2007.2007.

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Abstract Results from in vitro investigations and recent data obtained in patients with drug-induced cytopenia or myelodysplasia suggest that leukotrienes may be involved in mediating some of the actions of granulocyte-macrophage colony-stimulating factor (GM-CSF). In the present study, the possible role of leukotrienes was further characterized in 21 healthy individuals to avoid modification of response to GM-CSF by disease-specific variables. The effects of two different preparations of human recombinant GM-CSF, ie, glycosylated GM- CSF as expressed in a Chinese hamster ovary carcinoma (CHO)

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Denzlinger, C., W. Tetzloff, HH Gerhartz, et al. "Differential activation of the endogenous leukotriene biosynthesis by two different preparations of granulocyte-macrophage colony-stimulating factor in healthy volunteers." Blood 81, no. 8 (1993): 2007–13. http://dx.doi.org/10.1182/blood.v81.8.2007.bloodjournal8182007.

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Results from in vitro investigations and recent data obtained in patients with drug-induced cytopenia or myelodysplasia suggest that leukotrienes may be involved in mediating some of the actions of granulocyte-macrophage colony-stimulating factor (GM-CSF). In the present study, the possible role of leukotrienes was further characterized in 21 healthy individuals to avoid modification of response to GM-CSF by disease-specific variables. The effects of two different preparations of human recombinant GM-CSF, ie, glycosylated GM- CSF as expressed in a Chinese hamster ovary carcinoma (CHO) cell lin

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Williams, J. D., J. L. Robin, R. A. Lewis, T. H. Lee, and K. F. Austen. "Generation of leukotrienes by human monocytes pretreated with cytochalasin B and stimulated with formyl-methionyl-leucyl-phenylalanine." Journal of Immunology 136, no. 2 (1986): 642–48. http://dx.doi.org/10.4049/jimmunol.136.2.642.

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Abstract The N-formylated tripeptide N-formyl-methionyl-leucyl-phenylalanine (FMLP) initiated the generation of immunoreactive C-6 sulfidopeptide leukotrienes and of leukotriene B4 (LTB4) in a dose-dependent manner from monolayers of human monocytes pretreated for 10 min with 5 micrograms/ml of cytochalasin B. The EC50 for the immunoreactive C-6 sulfidopeptide leukotrienes was 10(-8) M FMLP and for immunoreactive LTB4 was 5 X 10(-8) M FMLP. The maximal response to FMLP occurred within 10 min, and the sum of the two classes of leukotrienes generated was about 1/6 that obtained from monocytes st

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Fauler, Joachim, Dimitrios Tsikas, Michael Holch, et al. "Enhanced urinary excretion of leukotriene E4 by patients with multiple trauma with or without adult respiratory distress syndrome." Clinical Science 80, no. 5 (1991): 497–504. http://dx.doi.org/10.1042/cs0800497.

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1. The aim of the present study was to evaluate the systemic synthesis of cysteinyl leukotrienes in patients with multiple trauma. In order to do this, the urinary excretion of leukotriene E4 was assessed in the first 10 days after trauma. 2. Leukotriene E4 was unequivocally identified by g.c.-m.s. in the urine of healthy subjects and patients with multiple trauma after its conversion to 5-hydroxyeicosanoic acid. Leukotriene E4 was routinely isolated from 24 h urine samples by solid-phase extraction followed by reverse-phase h.p.l.c. and was subsequently quantified by r.i.a. 3. Healthy subject

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Medeiros, Alexandra I., Anderson Sá-Nunes, Edson G. Soares, Camila M. Peres, Célio L. Silva, and Lúcia H. Faccioli. "Blockade of Endogenous Leukotrienes Exacerbates Pulmonary Histoplasmosis." Infection and Immunity 72, no. 3 (2004): 1637–44. http://dx.doi.org/10.1128/iai.72.3.1637-1644.2004.

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ABSTRACT Leukotrienes are classical mediators of inflammatory response. New aspects of leukotriene function have recently been described. We examine here the previously unreported role that leukotrienes play in the regulation of cytokines in a murine model of histoplasmosis. We demonstrate that administration of MK 886, a leukotriene synthesis inhibitor, caused Histoplasma capsulatum-infected mice to die by the day 15 of infection, whereas the correlating death rate in untreated infected mice was 0%. Treating infected animals with MK 886 inhibited leukotriene synthesis but increased leukocyte

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Chilton, F. H. "Potential phospholipid source(s) of arachidonate used for the synthesis of leukotrienes by the human neutrophil." Biochemical Journal 258, no. 2 (1989): 327–33. http://dx.doi.org/10.1042/bj2580327.

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The present study has employed two approaches to address the question of whether there are specific phospholipid sources of arachidonate used for leukotriene biosynthesis in the human neutrophil. Firstly, g.c.-m.s. analysis indicated that arachidonate was lost from all major arachidonate-containing phospholipid subclasses during cell activation with ionophore A23187. On a molar basis, the rank order of breakdown among the three major phospholipids was: 1-alk-1-enyl-2-arachidonoyl-sn-glycero-3-phosphoethanolamine greater than 1-alkyl-2-arachidonoyl-sn-3-phosphocholine greater than 1-acyl-2-arac

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Ali, A., A. W. Ford-Hutchinson, and D. W. Nicholson. "Activation of protein kinase C down-regulates leukotriene C4 synthase activity and attenuates cysteinyl leukotriene production in an eosinophilic substrain of HL-60 cells." Journal of Immunology 153, no. 2 (1994): 776–88. http://dx.doi.org/10.4049/jimmunol.153.2.776.

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Abstract An eosinophilic substrain of HL-60 cells (HL-60#7) predominantly synthesized cysteinyl leukotrienes after stimulation with the calcium ionophore A23187. Activation of protein kinase C (PKC) by phorbol 12-myristate 13-acetate (PMA) specifically attenuated cysteinyl leukotriene production without affecting the biosynthesis of non-cysteinyl leukotrienes. The inhibition of cysteinyl leukotriene biosynthesis was prevented only by specific PKC inhibitors (staurosporine and bisindolylmaleimide) but not by inhibitors of tyrosine kinases (genistein, tyrphostin 47, and herbimycin A), protein ki

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Freedman, Stephen M., John L. Wallace, and Eldon A. Shaffer. "Characterization of leukotriene-induced contraction of the guinea-pig gallbladder in vitro." Canadian Journal of Physiology and Pharmacology 71, no. 2 (1993): 145–50. http://dx.doi.org/10.1139/y93-020.

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Metabolites of arachidonic acid like prostaglandins have an established role in the pathogenesis of gallstone formation and cholecystitis, but any contribution by leukotrienes is less clear. Leukotrienes might contribute to the disease process by contracting the inflamed and (or) obstructed gallbladder, resulting in further inflammatory damage and biliary pain. To better define the role of leukotrienes, we assessed their effects on gallbladder contracility in vitro. Both leukotriene C4 (LTC4) and D4 (LTD4) had a concentration-dependent excitatory effect on guinea-pig gallbladder smooth muscle.

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Mygind, N., R. Dahl, and H. Bisgaard. "Leukotrienes, leukotriene receptor antagonists, and rhinitis." Allergy 55, no. 5 (2000): 421–24. http://dx.doi.org/10.1034/j.1398-9995.2000.00113.x.

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Empey, Lonnie R., Keith Walker, and Richard N. Fedorak. "Indomethacin worsens and a leukotriene biosynthesis inhibitor accelerates mucosal healing in rat colitis." Canadian Journal of Physiology and Pharmacology 70, no. 5 (1992): 660–68. http://dx.doi.org/10.1139/y92-084.

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The implication of leukotrienes as mediators of inflammation and recent evidence that prostaglandin analogues provide a beneficial effect during experimental colitis led to the speculation that (i) leukotrienes may be injurious and (ii) prostaglandins may be protective to colonic mucosa. Using a 2% acetic acid induced rat colitis model, we administered specific cyclooxygenase (indomethacin) and leukotriene biosynthesis inhibitors (MK-886) to examine the effect of endogenous prostaglandins and leukotrienes on colonic macroscopic injury, mucosal inflammation as measured by myeloperoxidase activi

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Jackson, Sarah E., John W. Holloway, Jane A. Warner, and Anthony P. Sampson. "Interleukin-13, but Not Indomethacin, Increases Cysteinyl-Leukotriene Synthesis in Human Lung Macrophages." Journal of Allergy 2012 (October 29, 2012): 1–6. http://dx.doi.org/10.1155/2012/348741.

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Aspirin-exacerbated respiratory disease (AERD) is associated with constitutively elevated synthesis of bronchoconstrictor cysteinyl-leukotrienes, associated with increased expression of leukotriene (LT)C4 synthase and Th2 cytokines and airway eosinophilia. We examined whether interleukin-13 can increase LTC4 synthase gene transcription and cysteinyl-leukotriene synthesis in macrophages isolated from resected human lung tissue and whether an NSAID (indomethacin) can trigger further cysteinyl-leukotriene synthesis in these cells. Overnight culture of human lung macrophages with IL-13 (10 ng/mL)

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34

Mansour, Mahmoud, Nabil Farouk, Abbas El Maragy, Ibrahim Radwan, and Omar El-Ahmady. "Elevated Plasma Level of Leukotrienes in Bronchial Asthma Patients: A Possible Clinical Relevance." Disease Markers 12, no. 2 (1994): 117–22. http://dx.doi.org/10.1155/1994/121453.

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Plasma from bronchial asthma patients and healthy controls was investigated for the content of lipoxygenase products. After lipid extraction using SEP-PAK C18Cartridges, the lipoxygenase products were measured by Enzyme-Immunoassay. Elevated chemotactic B4 was found in plasma from asthmatic patients with mean value (483±75) pmoUL, while the mean value in normal healthy donors was (140± 12.1) pmol/L (M±SE). The levels of spasmogenic cysteinyl containing leukotrienes were also very high in the bronchial asthma patients. Elevations of leukotriene B4and cysteinyl containing leukotrienes were detec

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Mancuso, Peter, Patrick Nana-Sinkam, and Marc Peters-Golden. "Leukotriene B4 Augments Neutrophil Phagocytosis of Klebsiella pneumoniae." Infection and Immunity 69, no. 4 (2001): 2011–16. http://dx.doi.org/10.1128/iai.69.4.2011-2016.2001.

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ABSTRACT Neutrophils play a critical role in the clearance of bacteria from the lung and other organs by their capacity for phagocytosis and killing. Previously, we identified an important role for the leukotrienes in rat alveolar macrophage phagocytosis ofKlebsiella pneumoniae. In this report, we explored the possibility that the leukotrienes play an important role in phagocytosis by neutrophils as well. Inhibition of endogenous leukotriene synthesis by 5-lipoxygenase knockout in mice or by pharmacologic means in human peripheral blood neutrophils attenuated phagocytosis of opsonized K. pneum

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36

Spurney, R. F., S. Ibrahim, D. Butterly, P. E. Klotman, F. Sanfilippo, and T. M. Coffman. "Leukotrienes in renal transplant rejection in rats. Distinct roles for leukotriene B4 and peptidoleukotrienes in the pathogenesis of allograft injury." Journal of Immunology 152, no. 2 (1994): 867–76. http://dx.doi.org/10.4049/jimmunol.152.2.867.

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Abstract To investigate the role of leukotrienes in renal allograft rejection, we studied the effects of specific leukotriene inhibitors in a rat kidney transplant model. The enhanced renal production of leukotrienes observed in allograft recipients was reduced in a dose-dependent manner by the specific 5-lipoxygenase inhibitor MK886. This suppression of leukotriene production caused a substantial improvement in renal function. Inhibition of 5-lipoxygenase also reduced the severity of vascular inflammation and endothelial injury in allografts, and profoundly inhibited expression of donor MHC c

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37

Draber, Petr, Tomas Paulenda, Pavol Utekal, et al. "Production of leukotriene signaling mediators is limited by ORMDL3/serine palmitoyltransferase/5-lipoxygenase crosstalk." Journal of Immunology 204, no. 1_Supplement (2020): 152.18. http://dx.doi.org/10.4049/jimmunol.204.supp.152.18.

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Abstract Leukotrienes and sphingolipids are critical lipid mediators participating in cellular signal transduction and development of various diseases. Metabolic pathways initiating production of these lipid mediators involve 5-lipoxygenase (5-LO)-mediated conversion of arachidonic acid to leukotrienes and serine palmitoyltransferase (SPT) de novo synthesis of sphingolipids. Previous studies showed that endoplasmic reticulum membrane protein ORMDL3 inhibits the activity of SPT and sphingolipid synthesis. However, the role of ORMDL3 in synthesis of leukotrienes is not known. In this study, we u

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Hirata, K., K. Maghni, P. Borgeat, and P. Sirois. "Guinea pig alveolar eosinophils and macrophages produce leukotriene B4 but no peptido-leukotriene." Journal of Immunology 144, no. 5 (1990): 1880–85. http://dx.doi.org/10.4049/jimmunol.144.5.1880.

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Abstract The metabolism of arachidonic acid (AA) was investigated in purified guinea pig alveolar eosinophils and macrophages. Alveolar eosinophils produced 12S-hydroxy-5,8,10-heptadecatraenoic acid (HHT) and small amounts only of 5-lipoxygenase products when stimulated by AA (10 microM) or ionophore A23187 (2 microM). However, when the cell suspensions were stimulated with both AA and A23187, the cells produced HHT, leukotriene (LT) B4, and 5S-hydroxy-6,8,11,14-eicosatetraenoic acid, whereas LTC4, D4, and E4 were undetectable. Similarly, alveolar macrophages stimulated with A23187 produced HH

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Kiwak, Kevin J., Michael A. Moskowitz, and Lawrence Levine. "Leukotriene production in gerbil brain after ischemic insult, subarachnoid hemorrhage, and concussive injury." Journal of Neurosurgery 62, no. 6 (1985): 865–69. http://dx.doi.org/10.3171/jns.1985.62.6.0865.

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✓ A leukotriene-like immunoreactivity was measured by radioimmunoassay in the gerbil forebrain following ischemia and reperfusion, subarachnoid hemorrhage (SAH), or nonlethal concussive brain injury. In each paradigm an increase in immunoreactivity levels was found. Peak levels were reached 15 to 30 minutes after each insult, and slowly returned to baseline over the next 24 hours. The study supports the suggestion that cerebral vessels and circulating blood are capable of producing leukotrienes, and that a major source of production is a nonvascular component within gray matter, possibly the c

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Runarsson, Gudmundur, Anquan Liu, Yilmaz Mahshid, et al. "Leukotriene B4 plays a pivotal role in CD40-dependent activation of chronic B lymphocytic leukemia cells." Blood 105, no. 3 (2005): 1274–79. http://dx.doi.org/10.1182/blood-2004-07-2546.

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AbstractBiosynthesis of leukotrienes (LTs) occurs in human myeloid cells and B lymphocytes. However, the function of leukotrienes in B lymphocytes is unclear. Here, we report that B-cell chronic lymphocytic leukemia (B-CLL) cells produce leukotriene B4, and that specific leukotriene biosynthesis inhibitors counteracted CD40-dependent activation of B-CLL cells. Studies on the expression of the high-affinity receptor for LTB4 (BLT1) by flow cytometry analysis showed that the receptor was expressed, to a varying degree, in all investigated B-CLL clones. At a concentration of 100 nM, the drugs BWA

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41

Riccioni, Graziano, and Magnus Bäck. "Leukotrienes as Modifiers of Preclinical Atherosclerosis?" Scientific World Journal 2012 (2012): 1–6. http://dx.doi.org/10.1100/2012/490968.

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Preclinical atherosclerosis represents a crucial period associated with several pathophysiological reactions in the vascular wall. Failure to diagnose preclinical atherosclerosis at this stage misses a major opportunity to prevent the long-term consequences of this disease. Surrogate biological and structural vascular markers are available to determine the presence and the extension of preclinical vascular injury in the general population. Examples of surrogate markers are carotid intima media thickness and biomarkers including high-sensitivity C-reactive protein, cell adhesion molecules and m

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42

ZHANG, Ying-Yi, Jennifer L. WALKER, Annong HUANG, et al. "Expression of 5-lipoxygenase in pulmonary artery endothelial cells." Biochemical Journal 361, no. 2 (2002): 267–76. http://dx.doi.org/10.1042/bj3610267.

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Increased expression of 5-lipoxygenase (5LO) in pulmonary artery endothelial cells (PAECs) has been observed in disease states such as pulmonary hypertension and allergen challenge. To understand the function of endothelial 5LO, we examined the expression of this enzyme in normally cultured human PAECs and its characteristics when overexpressed. A small amount of 5LO message and protein was detected by reverse-transcriptase-mediated PCR (RT—PCR) and Western blotting in PAECs. Sequencing of the RT—PCR products that overlapped the entire coding region of 5LO mRNA indicated that the sequence of P

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43

Bautz, Frank, Claudio Denzlinger, Lothar Kanz, and Robert Möhle. "Chemotaxis and transendothelial migration of CD34+hematopoietic progenitor cells induced by the inflammatory mediator leukotriene D4 are mediated by the 7-transmembrane receptor CysLT1." Blood 97, no. 11 (2001): 3433–40. http://dx.doi.org/10.1182/blood.v97.11.3433.

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Recent studies suggest that bone marrow (BM)–derived chemotactic mediators such as chemokines play key roles in hematopoietic stem cell trafficking. Lipid mediators, particularly leukotrienes, are involved in leukocyte chemotaxis during inflammation but have also been detected in the normal BM. Therefore, the effects of leukotrienes on hematopoietic progenitor cells were analyzed. Cysteinyl leukotrienes, particularly leukotriene D4 (LTD4), induced strong intracellular calcium fluxes and actin polymerization in mobilized and BM CD34+ progenitors. Chemotaxis and in vitro transendothelial migrati

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44

Mizernitskiy, Yu L., and A. I. Petrova. "Montelukast: results and prospects for applications in pediatric practice." Meditsinskiy sovet = Medical Council, no. 1 (February 26, 2024): 82–88. http://dx.doi.org/10.21518/ms2024-026.

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The Centers for Disease Control and Prevention reports that more than 4 million children have been diagnosed with asthma. Currently, there is no treatment that could prevent the development of asthma or change its natural course over long-term follow-up. However, the disease can be controlled using treatments used in clinical practice. For persistent asthma in children aged 5 years and younger, low doses of inhaled glucocorticosteroids are recommended, as well as the administration of montelukast, a leukotriene receptor antagonist. In addition, montelukast is prescribed to patients with allerg

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45

Soifer, S. J., R. D. Loitz, C. Roman, and M. A. Heymann. "Leukotriene end organ antagonists increase pulmonary blood flow in fetal lambs." American Journal of Physiology-Heart and Circulatory Physiology 249, no. 3 (1985): H570—H576. http://dx.doi.org/10.1152/ajpheart.1985.249.3.h570.

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The factors responsible for maintaining the normally low pulmonary blood flow and high pulmonary vascular resistance in the fetus are not well understood. Since leukotrienes are potent pulmonary vasoconstrictors in many adult animal species, we determined whether leukotrienes were perhaps involved in the control of the fetal pulmonary circulation by studying the effects of putative leukotriene end organ antagonists in two groups of fetal lambs. In six fetal lambs studied at 130-134 days gestation, FPL 55712 increased pulmonary blood flow by 61% (P less than 0.05) and reduced pulmonary vascular

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46

Ford-Hutchinson, A. W., P. Tagari, S. V. Ching, C. A. Anderson, J. B. Coleman, and C. P. Peter. "Chronic leukotriene inhibition in the rat fails to modify the toxicological effects of a cyclooxygenase inhibitor." Canadian Journal of Physiology and Pharmacology 71, no. 10-11 (1993): 806–10. http://dx.doi.org/10.1139/y93-120.

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A 5-week study was carried out in rats using a leukotriene biosynthesis inhibitor (MK-886; 3-[1-(4-chlorobenzyl)-3-t-butylthio-5-isopropylindol-2-yl]-2,2-dimethylpropanoic acid) at a dose of 300 mg∙kg−1∙day−1, this being sufficient to produce > 90% inhibition of ex vivo leukotriene B4 synthesis in rat blood, and a cyclooxygenase inhibitor (indomethacin, 4 and 6 mg∙kg−1∙day−1) to ascertain whether inhibition of leukotriene biosynthesis would potentiate or inhibit the toxicity associated with the administration of nonsteroidal anti-inflammatory drugs (NSAIDs), in particular the gastrointestin

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47

Claesson, Hans-Erik, Gudmundur Runarsson, Anquan Liu, et al. "Leukotriene B4 Plays a Pivotal Role in CD40 Dependent Activation of Chronic B Lymphocytic Leukemia Cells." Blood 104, no. 11 (2004): 4808. http://dx.doi.org/10.1182/blood.v104.11.4808.4808.

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Abstract Biosynthesis of leukotrienes occurs in human myeloid cells and B lymphocytes. However, the function of leukotrienes in B lymphocytes is unclear. Here we report that B-cell chronic lymphocytic leukemia (B-CLL) cells produce leukotriene (LT) B4 and that specific leukotriene biosynthesis inhibitors counteracted CD40-dependent activation of B-CLL cells. Studies on the expression of the high affinity receptor for LTB4 (BLT1) by flow cytometry analysis showed that the receptor was expressed, to a varying degree, in all investigated B-CLL clones. The drugs BWA4C (a specific 5-lipoxygenase in

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48

Marschallinger, Julia, Barbara Altendorfer, Edward Rockenstein, et al. "The Leukotriene Receptor Antagonist Montelukast Reduces Alpha-Synuclein Load and Restores Memory in an Animal Model of Dementia with Lewy Bodies." Neurotherapeutics 17, no. 3 (2020): 1061–74. http://dx.doi.org/10.1007/s13311-020-00836-3.

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Abstract Dementia with Lewy bodies (DLB) represents a huge medical need as it accounts for up to 30% of all dementia cases, and there is no cure available. The underyling spectrum of pathology is complex and creates a challenge for targeted molecular therapies. We here tested the hypothesis that leukotrienes are involved in the pathology of DLB and that blocking leukotrienes through Montelukast, a leukotriene receptor antagonist and approved anti-asthmatic drug, might alleviate pathology and restore cognitive functions. Expression of 5-lipoxygenase, the rate-limiting enzyme for leukotriene pro

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Byrum, Robert S., Jennifer L. Goulet, Richard J. Griffiths, and Beverly H. Koller. "Role of the 5-Lipoxygenase–activating Protein (FLAP) in Murine Acute Inflammatory Responses." Journal of Experimental Medicine 185, no. 6 (1997): 1065–76. http://dx.doi.org/10.1084/jem.185.6.1065.

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Leukotrienes are potent inflammatory mediators synthesized from arachidonic acid (AA) predominately by cells of myeloid origin. The synthesis of these lipids is believed to be dependent not only on the expression of the enzyme 5-lipoxygenase (5-LO), which catalyzes the first steps in the synthesis of leukotrienes, but also on expression of a nuclear membrane protein termed the 5-LO–activating protein (FLAP). To study the relationship of these two proteins in mediating the production of leukotrienes in vivo and to determine whether the membrane protein FLAP has additional functions in various i

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Cassin, S., K. R. Stenmark, G. Gause, L. M. Zapp, H. Kuck, and J. Y. Westcott. "Leukotrienes and prostaglandins in fetal lung liquid." Journal of Applied Physiology 68, no. 5 (1990): 2214–22. http://dx.doi.org/10.1152/jappl.1990.68.5.2214.

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Several recent studies have suggested that peptidoleukotrienes are involved in or responsible for the pulmonary pressor response to hypoxia as well as the normally high pulmonary vascular resistance of fetal lambs. The present studies were carried out to test these hypotheses. Fetal lambs were prepared with indwelling vascular catheters and tracheal catheters for access to lung liquid. We measured lung liquid levels of leukotrienes C4 (LTC4) and D4 (LTD4) in control unanesthetized fetal lambs with blood gases and pH in the normal range. In the control series, LTC4 and LTD4 were either not dete

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