Effect of prostaglandin E2 on eicosanoid release by human bronchial biopsy specimens from normal and inflamed mucosa.

Schäfer, Dirk; Lindenthal, U.; Wagner, Mary H.; Bölcskei, P. L.; Baenkler, H W

doi:10.1136/thx.51.9.919

Cited by 53 publications

(52 citation statements)

References 33 publications

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“…combined drugs of PGE 2 and 5-lipoxygenase inhibitors or leukotriene-receptor antagonists. The bronchoprotective effect of inhaled PGE 2 [4,16] is most likely mediated by direct inhibition of pLT release as it has been recently reported for human bronchial biopsy specimens [24]. When AIAs are challenged with aspirin, pLT release increases most likely because of further reduction of inhibitory PGE 2 and/or partially by "shunting" of arachidonic acid metabolism and/or release of other bronchoconstrictive mediators.…”

Section: Discussionmentioning

confidence: 69%

“…-5 M) of PGE 2 , dibutyryl-cAMP or the 5-lipoxygenase inhibitor caffeic acid [24]. In normal subjects, PGE 2 reduced pLT release in a dose-dependent fashion with 78% inhibition of arachidonic acid-induced pLT release at 10 -5 M PGE 2 .…”

Section: ±10mentioning

confidence: 94%

“…For more detailed data on cross-reactivities for the other eicosanoids tested, see [22,23]. The pLT-and PGE 2 -EIA were performed according to the protocols published recently [24], diluting standard and samples in RPMI-1640. The intra-and interassay variance for pLT-EIA were 9% and 7.5%, respectively and for PGE 2 -EIA 8% and 6%, respectively.…”

Section: Quantification Of Mediatorsmentioning

confidence: 99%

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Dynamics of eicosanoids in peripheral blood cells during bronchial provocation in aspirin-intolerant asthmatics

Schäfer

Schmid²,

Göde³

et al. 1999

Eur Respir J

102

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The underlying mechanisms of bronchoconstriction in aspirin-intolerant asthmatics (AIAs) are still unknown, but the hypothesis of an altered metabolism of arachidonic acid is generally accepted. So far, no in vitro test for aspirin intolerance is available. The hypothesis that the profile of eicosanoid mediators is changed in AIA-even before aspirin challenge was tested.The release of prostaglandin E 2 (PGE 2 ), peptidoleukotrienes and histamine was measured using competitive enzyme immunoassays in 10 asthmatics with a history of aspirin intolerance, 10 controls and eight aspirin-tolerant asthmatics (ATAs) before and after bronchial provocation with lysine-aspirin.Comparing basal release of eicosanoids before challenge, peptidoleukotrienes were significantly elevated and PGE 2 was vastly reduced in AIAs, whereas ATAs had elevated basal peptidoleukotrienes but only slightly reduced basal PGE 2 . The decrease in forced expiratory volume in one second (FEV1) was not associated with changes in histamine release. After aspirin challenge, there was a massive increase of already elevated peptidoleukotrienes in AIAs, but not in ATAs. Arachidonic acid-induced PGE 2 release in AIAs was not significantly changed, whereas it was significantly reduced in ATAs and healthy controls. Histamine release was unaffected by aspirin challenge in all three groups.There is a typically altered profile of eicosanoids in aspirin-intolerant asthmatics which could make in vitro diagnosis of aspirin intolerance possible. Eur Respir J 1999; 13: 638±646.

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Section: Discussionmentioning

confidence: 69%

Section: ±10mentioning

confidence: 94%

Section: Quantification Of Mediatorsmentioning

confidence: 99%

See 1 more Smart Citation

Dynamics of eicosanoids in peripheral blood cells during bronchial provocation in aspirin-intolerant asthmatics

Schäfer

Schmid²,

Göde³

et al. 1999

Eur Respir J

102

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“…Using a highly sensitive and specific competitive enzyme-linked immunosorbent assay (ELISA) with a monoclonal antibody from clone E2R1 (Schafer et al, 1996), PGE 2 was detected in culture supernatants of HL-60 cells and primary AML blasts with or without 0.15 g/ml DOX or 1 M arachidonic acid as a positive control. The detection limit for PGE 2 was 3 pg/ml of a 96-well microculture plate.…”

Section: Methodsmentioning

confidence: 99%

Impact of the Cyclooxygenase System on Doxorubicin-Induced Functional Multidrug Resistance 1 Overexpression and Doxorubicin Sensitivity in Acute Myeloid Leukemic HL-60 Cells

Puhlmann¹,

Ziemann²,

Ruedell³

et al. 2004

J Pharmacol Exp Ther

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Multidrug resistance (MDR), a challenge in treating childhood acute myeloid leukemia (AML), is frequently associated with decreased drug accumulation caused by multidrug transporter MDR1. Doxorubicin, an important anti-AML drug, is a known MDR1 substrate and inducer. Its cytostatic efficacy is thus limited by MDR1 overexpression. A recent study demonstrated cyclooxygenase-2-dependent, prostaglandin E 2 (PGE 2 )-mediated regulation of mdr1b expression in primary rat hepatocyte cultures. Cyclooxygenase-2 expression is increased in several malignancies and considered a negative prognostic factor. Our study focused on cyclooxygenase system's impact on drug-induced MDR1 overexpression in AML cells. As a prerequisite, coexpression of MDR1 and cyclooxygenase-2 mRNA in HL-60 cells and primary AML blasts was demonstrated by Northern blot. Interestingly, incubation of AML cells with doxorubicin not only induced functionally active MDR1 overexpression but also mediated increased cyclooxygenase-2 mRNA and protein expressions with subsequent PGE 2 release (determined by flow cytometry, rhodamine123 efflux assay, reverse transcription-polymerase chain reaction, and enzyme-linked immunosorbent assay). After preincubation and subsequent parallel treatment with the cyclooxygenase-2-preferential inhibitor meloxicam, doxorubicin-induced MDR1 overexpression and function were reduced (maximally at 0.1-0.5 M meloxicam), whereas cytostatic efficacy of doxorubicin in 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide assays was significantly increased by up to 78 (HL-60) and 30% (AML blasts) after 72 h of doxorubicin treatment. In HL-60 cells, meloxicam-dependent effect on doxorubicin cytotoxicity was neutralized by PGE 2 preincubation. In conclusion, the cyclooxygenase system, especially the cyclooxygenase-2 isoform, might be involved in regulating doxorubicin-induced MDR1 overexpression in AML cells, with PGE 2 seeming to be a mediating factor. Cyclooxygenase inhibitors thus bear promise to overcome MDR in AML and improve therapy.

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“…Blood cells were analysed for eicosanoid release upon in vitro modi cation as published (18,19,25,31,32) . In brief, aliquots of peripheral white blood cells were incubated for 20 minutes with diluents, with and without arachidonic acid, acetylsalicylic acid or neuropeptide.…”

Section: Laboratory Ndings In Vitro Studymentioning

confidence: 99%

Eicosanoid imbalance correlates in vitro with the pattern of clinical symptoms of Samter ́s triad

Forster¹,

Strathmann²,

Schafer³

et al. 2013

Rhin

Self Cite

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SummaryBackground: Hypersensitivity to non-steroidal anti-in ammatory drugs (NSAIDs) is often associated with chronic rhinosinusitis (CRS), nasal polyps (CRSwNP) and asthma, together known as Samter´s triad. The disease is characterised by eicosanoid imbalance. In our study, we determined clinical and laboratory parameters in respect of three groups of patients: 1) CRSwNP, 2) CRSwNP and asthma (CRSwNP-A), and 3) CRSwNP with asthma and NSAID-triggered hypersensitivity (CRSwNP-AA). Our main goal was to improve the characterisation of the stages of development in Samter´s triad, pointing to the homogeneous or heterogeneous course of disease. Methodology:Forty-three patients (10 CRSwNP, 14 CRSwNP-A, 19 CRSwNP-AA) and 10 control subjects were included in the study. Nasal assessment using the CRS visual analogue score, endoscopy-and computer tomography scores, allergy tests, analysis of sinus surgeries, asthma severity and in vitro functional eicosanoid tests (FET) with peripheral blood leucocytes were performed. Results:The scores re ecting CRS symptoms such as nasal congestion, nasal discharge and smell impairment di ered between the patients groups re ecting the severity of disease (CRSwNP-AA > CRSwNP-A > CRSwNP). Eicosanoid imbalance correlated with nasal congestion, nasal discharge and loss of smell. Conclusion:The data presented support the hypothesis of the continuous development of NSAID-triggered hypersensitivity, culminating in Samter's triad.

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Effect of prostaglandin E2 on eicosanoid release by human bronchial biopsy specimens from normal and inflamed mucosa.

Cited by 53 publications

References 33 publications

Dynamics of eicosanoids in peripheral blood cells during bronchial provocation in aspirin-intolerant asthmatics

Dynamics of eicosanoids in peripheral blood cells during bronchial provocation in aspirin-intolerant asthmatics

Impact of the Cyclooxygenase System on Doxorubicin-Induced Functional Multidrug Resistance 1 Overexpression and Doxorubicin Sensitivity in Acute Myeloid Leukemic HL-60 Cells

Eicosanoid imbalance correlates in vitro with the pattern of clinical symptoms of Samter ́s triad

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