Prostaglandins inhibit inflammatory mediator release from rat mast cells

Hogaboam, Cory M.; Bissonnette, Élyse; Chin, Beth C.; Befus, A. Dean; Wallace, John L.

doi:10.1016/0016-5085(93)90843-2

Cited by 119 publications

(51 citation statements)

References 31 publications

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“…This is consistent with the findings reported by Leal-Berumen et al (23), using rat peritoneal mast cells, and with results obtained using BMMCs and IL-3-dependent mast cell lines (19,20). Our results contrast sharply, however, with other studies that showed that PGE 2 could inhibit the release of mediators from both rat peritoneal mast cells (24,25) and human lung mast cells (26,27). It is likely that at least some of these differences reflect the use of different mast cell populations in these studies.…”

Section: Discussioncontrasting

confidence: 99%

Receptors and Signaling Mechanisms Required for Prostaglandin E2-Mediated Regulation of Mast Cell Degranulation and IL-6 Production

Nguyen¹,

Solle

Audoly

et al. 2002

The Journal of Immunology

102

108

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Mast cells are implicated in the pathogenesis of a broad spectrum of immunological disorders. These cells release inflammatory mediators in response to a number of stimuli, including IgE-Ag complexes. The degranulation of mast cells is modified by PGs. To begin to delineate the pathway(s) used by PGs to regulate mast cell function, we examined bone marrow-derived mast cells (BMMC) cultured from mice deficient in the EP1, EP2, EP3, and EP4 receptors for PGE2. Although BMMCs express all four of these PGE2 receptors, potentiation of Ag-stimulated degranulation and IL-6 cytokine production by PGE2 is dependent on the EP3 receptor. Consistent with the coupling of this receptor to Gαi, PGE2 activation of the EP3 receptor leads to both inhibition of adenylate cyclase and increased intracellular Ca2+. The magnitude of increase in intracellular Ca2+ induced by EP3 activation is similar to that observed after activation of cells with IgE and Ag. Although PGE alone is not sufficient to initiate BMMC degranulation, stimulation of cells with PGE along with PMA induces degranulation. These actions are mediated by the EP3 receptor through signals involving Ca2+ mobilization and/or decreased cAMP levels. Accordingly, these studies identify PGE2/EP3 as a proinflammatory signaling pathway that promotes mast cell activation.

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Section: Discussioncontrasting

confidence: 99%

Receptors and Signaling Mechanisms Required for Prostaglandin E2-Mediated Regulation of Mast Cell Degranulation and IL-6 Production

Nguyen¹,

Solle

Audoly

et al. 2002

The Journal of Immunology

102

108

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“…49) The protective action of prostaglandins is mediated by increased production of mucus and bicarbonate secretion, 50) modulation of gastric acid secretion, 51) inhibition of the release of inflammatory mediators by mast cells, 52) and the maintenance of gastric blood flow during exposure. The data are the meanϮS.D.…”

Section: Resultsmentioning

confidence: 99%

Gastric Antiulcer Activity of <i>Syngonanthus arthrotrichus</i> S<small>ILVEIRA</small>

Batista

Almeida

Magri

et al. 2004

Biological & Pharmaceutical Bulletin

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Syngonanthus arthrotrichus SILVEIRA (Eriocaulaceae) popularly know as "sempre-vivas mini-saia" is found chiefly in the Espinhaço mountain range in the Brazilian states of Bahia and Minas Gerais where it grows in rocky or sandy soil in areas of open vegetation. 1)The family Eriocaulaceae is complex and includes diverse herbaceous, monocotyledonous species which have miniature flowers grouped in clusters. These plants have inflorescences and scapes that retain the appearance of living structures when dried.2) Species of the genus Syngonanthus are of economic importance since they are exported as ornamental plants to various countries.Little is known about the ethnopharmacology of Syngonanthus species. Phytochemical studies have detected a variety of chemical constituents, 3,4) including flavonoids which have antiulcerogenic, antioxidant, 5) and immunostimulant actions. 6)Gastric and duodenal ulcers affect a large proportion of the world population and are induced by several factors, including stress, smoking, nutritional deficiencies, and ingestion of nonsteroidal anti-inflammatory drugs. 7,8) Protection of the gastric mucosa involves the factors such as acid-pepsin secretion, parietal cell activity, mucosal barrier, mucus secretion, blood flow, cell regeneration, and the release of endogenous protective agents, especially prostaglandins and epidermal growth factors. 9)Numerous approaches have been used to combat gastric ulcers, including the control of acid secretion, Helicobacter pylori level, and H ϩ /K ϩ -ATPase activity, in an attempt to reverse mucosal damage and inflammation. 10) In this context, extracts and active principles from plants could serve as leads for the development of new drugs.11) Flavonoids such as catechin, hypoletin, apigenin, luteolin, rugin, and genistein have antiulcer activity. 12-15)The objective of this study was to investigate the antiulcerogenic action of extracts from Syngonanthus arthrotrichus in ulcers induced by different agents in mice and rats and to examine the action mechanisms involved. Syngonanthus arthrotrichus SILVEIRA, popularly known as "sempre-vivas mini-saia," is found in mountains of the Espinhaço range in the Brazilian states of Bahia and Minas Gerais. Extracts of this species contain several constituents, including flavonoids which may have antiulcerogenic activity. An ethanolic extract (EEOH), and flavonoid-rich (FRF) and flavonoid-deficient (FDF) fractions obtained from the scapes of S. arthrotrichus were investigated for their ability to prevent ulceration of the gastric mucosa in mice and rats. In the ethanol/HCl-induced ulcer model, lansoprazole (30 mg/kg), EEOH (50, 100, 250 mg/kg) given orally protected the gastric mucosal against injury in mice by 79%, 78%, 73%, and 64% respectively. In the ethanol-induced gastric ulcer model in rats, the lansoprazole (30 mg/kg), FRF and FDF (100 mg/kg) significantly protected the gastric mucosal of rats by 65%, 38% and 25% respectively when compared with the negative control group. In indomethacin/ bethanechol-induced ga...

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“…[1][2][3][4][5][6][7][8] Increased leukotriene synthesis and release has been clearly demonstrated in aspirin sensitive asthmatic patients. 28 29 It is likely that leukotriene production is controlled by PGE 2 .…”

Section: Discussionmentioning

confidence: 99%

“…Prostaglandins of the E series (PGE), products of AA derived from the cyclo-oxygenase (COX) pathway, exert many anti-inflammatory eVects. They inhibit activation of neutrophils, basophils, monocytes, and mast cells [1][2][3][4][5][6] and production of interleukin (IL)-1, IL-2, tumour necrosis factor (TNF)-, and interferon (IFN)-. 7 8 The synthesis and release of leukotrienes is also likely to be downregulated by PGE.…”

mentioning

confidence: 99%

A six week double blind, placebo controlled, crossover study of the effect of misoprostol in the treatment of aspirin sensitive asthma

Wasiak¹,

Szmidt²

1999

Thorax

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Background-Prostaglandins of the E series and misoprostol (a stable analogue of prostaglandin E 1 ) prevent bronchoconstriction following aspirin ingestion or inhalation in subjects with aspirin sensitive asthma. A study was undertaken to investigate the influence of misoprostol on the course of aspirin induced asthma. Methods-A double blind, crossover, randomised, placebo controlled study was performed in 17 patients with aspirin sensitive asthma (13 women) aged 26-68 years. All subjects had aspirin sensitivity confirmed by means of oral aspirin or inhaled lysine aspirin challenge. Misoprostol (Cytotec, Searle, 800 or 1600 µg daily according to individual tolerance) or placebo were administered over a period of six weeks. Morning and evening peak expiratory flow rate (PEFR), 2 agonist use, asthma and rhinitis severity scores, and defaecation score were measured daily. At the beginning and end of each treatment period spirometric tests were performed and blood was taken for eosinophil count. Eight subjects took misoprostol at a dose of 800 µg and nine subjects at a dose of 1600 µg daily. Results-No diVerences were seen in asthma control between misoprostol and placebo except for the rhinorrhoea score which was lower on misoprostol during the period of the study. Conclusion-Misoprostol in a daily dose of 800 or 1600 µg does not significantly improve asthma control in subjects with aspirin sensitive asthma. (Thorax 1999;54:900-904)

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Prostaglandins inhibit inflammatory mediator release from rat mast cells

Cited by 119 publications

References 31 publications

Receptors and Signaling Mechanisms Required for Prostaglandin E2-Mediated Regulation of Mast Cell Degranulation and IL-6 Production

Receptors and Signaling Mechanisms Required for Prostaglandin E2-Mediated Regulation of Mast Cell Degranulation and IL-6 Production

Gastric Antiulcer Activity of <i>Syngonanthus arthrotrichus</i> S<small>ILVEIRA</small>

A six week double blind, placebo controlled, crossover study of the effect of misoprostol in the treatment of aspirin sensitive asthma

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