Purification and mass spectrometry identification of leukotriene D4 synthesized by human alveolar macrophages

Damon, Marie; Chavis, C.; Godard, P.; Michel, Françoise; Paulet, A. Crastes de

doi:10.1016/0006-291x(83)90337-6

Cited by 47 publications

(8 citation statements)

References 11 publications

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“…There is very little existing information on the regulation of PGE 2 receptor subtypes on inflammatory cells. Nonspecific stimuli such as LPS have been reported to upregulate PGE 2 receptor subtypes differentially in macrophages, 26,27 an effect that was antagonized by IFN-g. 27 Other studies 28,29 suggest that macrophages from patients with asthma may be *Data are expressed as means 6 SEMs of percentages of EP receptor 1 eosinophils from each group. The variability in parameters studied was analyzed with the Kruskal-Wallis test.…”

Section: Discussionmentioning

confidence: 99%

Expression of prostaglandin E2 receptor subtypes on cells in sputum from patients with asthma and controls: Effect of allergen inhalational challenge

Sun

O’Connor

Meng

et al. 2004

Journal of Allergy and Clinical Immunology

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Section: Discussionmentioning

confidence: 99%

Expression of prostaglandin E2 receptor subtypes on cells in sputum from patients with asthma and controls: Effect of allergen inhalational challenge

Sun

O’Connor

Meng

et al. 2004

Journal of Allergy and Clinical Immunology

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“…Immunological activation of human lung mast cells not only releases histamine but also leads to the synthesis and release of PGD2 (Holgate et al, 1984) and sulphidopeptide leukotrienes (MacGlashan et al, 1982). Although leukotrienes may also be released from other cells within the dispersed samples (Damon et al, 1983), the mast cell is the only source of PGD2 (Holgate et al, 1984). Our observation that SCG inhibits the release of PGD2 more effectively than that of histamine, therefore, reflects a differential inhibition of mediator release within the same cell population.…”

Section: Discussionmentioning

confidence: 99%

“…Although leukotrienes may also be released from other cells within the dispersed samples (Damon et al, 1983), the mast cell is the only source of PGD2 (Holgate et al, 1984). Our observation that SCG inhibits the release of PGD2 more effectively than that of histamine, therefore, reflects a differential inhibition of mediator release within the same cell population.…”

Section: Influence Ofdispersal Methodsmentioning

confidence: 99%

Inhibition of IgE‐dependent histamine release from human dispersed lung mast cells by anti‐allergic drugs and salbutamol

Church

Hiroi

1987

British J Pharmacology

251

121

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The ability of the anti‐allergic drugs, sodium cromoglycate (SCG), lodoxamide, traxanox, RU31156 and the β‐adrenoceptor agonist sulbutamol to inhibit IgE‐dependent histamine and prostaglandin D2 (PGD2) release was assessed using human dispersed lung mast cells. The anti‐allergic drugs were weak inhibitors of histamine release, high concentrations (100–1000 μm) producing < 35% inhibition. Salbutamol produced 39% inhibition at 10 μm. The efficacy of both SCG and salbutamol was inversely related to the concentration of anti‐IgE used for challenge and to the degree of histamine release. Rapid tachyphylaxis was observed with all anti‐allergic drugs but not with salbutamol. Cross‐tachyphylaxis was observed between SCG and the other anti‐allergic drugs, suggesting a common mechanism of action. No cross‐tachyphylaxis was observed between SCG and salbutamol. SCG was significantly (P < 0.001) more effective in inhibiting PGD2 than it was histamine release. Preferential inhibition of PGD2 compared with histamine release was less marked (P < 0.05) with salbutamol and not significant with the other anti‐allergic drugs. Mast cells dispersed by enzymatic digestion of human lung released more histamine on immunological challenge than mechanically dispersed cells obtained by fine chopping of tissue. Enzyme treatment of mechanically dispersed cells removed this difference. Enzymatically and mechanically dispersed cells responded similarly to the inhibitory effects of SCG and salbutamol. Our results suggest that salbutamol is a more effective inhibitor of mediator release from human lung mast cells than anti‐allergic drugs. However, with the low levels of mediator release achieved during an allergic reaction in man in vivo, both salbutamol and SCG are likely to be effective inhibitors of both preformed and newly generated mediators.

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“…However, it has been shown that LTC 4 is not the exclusive mediator of gastric injury caused by indomethacin (8). Cysteinyl leukotrienes, leukotrienes C 4 , D 4 , and E 4 (LTC 4 , LTD 4 , and LTE 4 ), are secreted mainly by eosinophils, mast cells, monocytes, and macrophages and perform a number of pathogenic actions during periods of inflammation (9,10). It has been reported by Konturek et al (11) that exogenous LTC 4 causes only mild cases of gastric mucosal injury, but greatly augments the mucosal lesions induced by various noxious agents such as ethanol, taurocholate, and aspirin or by stress.…”

Section: Introductionmentioning

confidence: 99%

Gastroprotective and Antioxidant Effects of Montelukast on Indomethacin-Induced Gastric Ulcer in Rats

Dengiz¹,

Odabaşoğlu

Halıcı

et al. 2007

J Pharmacol Sci

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Abstract. Montelukast, a selective reversible cysteinyl leukotriene D 4 -receptor (LTD 4 receptor) antagonist, is used in the treatment of asthma. We have investigated alterations in the glutathione (GSH) and activity levels of antioxidative enzymes [superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), and glutathione reductase (GR)] and myeloperoxidase (MPO), as markers of the ulceration process following oral administration of montelukast, lansoprazole, famotidine, and ranitidine, respectively, in rats with indomethacin-induced ulcers. In the present study, we found that 1) montelukast, lansoprazole, famotidine, and ranitidine all reduced the development of indomethacin-induced gastric damage, with this reduction occurring at a greater magnitude for montelukast, famotidine, and lansoprazole than for ranitidine; 2) montelukast and ranitidine both alleviated increases in the activity levels of CAT and GST enzymes resulting from gastric injury; 3) montelukast and ranitidine both ameliorated depressions in the GSH and activity levels of SOD and GR enzymes caused by indomethacin administration; and 4) all doses of montelukast, lansoprazole, and ranitidine decreased amplification of MPO activity resulting from induced gastric injuries. These results suggest that the gastroprotective effects of montelukast on indomethacin-induced ulcerations can be attributed to its ameliorating effect on oxidative damage and MPO activity.

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Purification and mass spectrometry identification of leukotriene D4 synthesized by human alveolar macrophages

Cited by 47 publications

References 11 publications

Expression of prostaglandin E2 receptor subtypes on cells in sputum from patients with asthma and controls: Effect of allergen inhalational challenge

Expression of prostaglandin E2 receptor subtypes on cells in sputum from patients with asthma and controls: Effect of allergen inhalational challenge

Inhibition of IgE‐dependent histamine release from human dispersed lung mast cells by anti‐allergic drugs and salbutamol

Gastroprotective and Antioxidant Effects of Montelukast on Indomethacin-Induced Gastric Ulcer in Rats

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