A monoclonal antibody against the sulfidopeptide leukotrienes LTC4, LTD4 and LTE4

Reinke, Margot; Hoppe, U.; Röder, Thomas; Bestmann, H. J.; Mollenhauer, Jürgen; Brune, Kay

doi:10.1016/0005-2760(91)90282-m

Cited by 17 publications

(12 citation statements)

References 13 publications

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“…The release of immunoreactive pLT, PGE 2 and histamine was quantified simultaneously for each sample in duplicates by highly sensitive and specific competitive enzyme immunoassays (EIA) using formerly established and validated monoclonal antibodies for pLT [22] and PGE 2 [23]. The cross-reactivities of the monoclonal pLTantibody were 95.7%, 100%, and 88.7% for leukotriene (LT)C 4 , LTD 4 , and LTE 4 , respectively, those for the monoclonal PGE 2 -antibody were 100% and 5.54% for PGE 2 and PGE 1 , respectively.…”

Section: Quantification Of Mediatorsmentioning

confidence: 99%

“…The cross-reactivities of the monoclonal pLTantibody were 95.7%, 100%, and 88.7% for leukotriene (LT)C 4 , LTD 4 , and LTE 4 , respectively, those for the monoclonal PGE 2 -antibody were 100% and 5.54% for PGE 2 and PGE 1 , respectively. 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.…”

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: Quantification Of Mediatorsmentioning

confidence: 99%

Section: Quantification Of Mediatorsmentioning

confidence: 99%

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 enzyme immuno assay must be carried out no later than 4 weeks. The CAST‐ELISA is based on the recognition of leukotrien C4 as well as its two metabolites (leukotrien D4 and leukotrien E4) by a single monoclonal antibody with the same sensitivity and specifity [5–9]. By means of the CAST‐ELISA all sulfidoleukotrienes can be measured generated by cellular antigen stimulation.…”

Section: Methodsmentioning

confidence: 99%

Case Report. Monascus purpureus—a new fungus of allergologic relevance

Hipler

Wigger‐Alberti

Bauer

et al. 2002

Mycoses

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Anaphylactic reactions to food containing allergens in the consumption or preparation of food are well known. However, allergy in the preparation of sausages has rarely been described. In the present study a 26-year-old-butcher was investigated who had a severe anaphylactic reaction developing sneezing, rhinitis, conjunctivitis, generalised pruritus, followed by widespread urticaria, Quincke's oedema and dyspnoe after starting to prepare sausages containing red yield rice. Red yield rice is produced by the fungus Monascus purpureus. It was the first time that Monascus purpureus could be shown as allergic agent by means of prick-to-prick test, Cellular Antigen Stimulation Test (CAST) and different immunoblots.

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“…Iscove's medium was obtained from Gibco (Karlsruhe, FRG). A monoclonal antibody directed against LTC 4 was kindly donated by Dr. M. Reinke (Universit~it Erlangen, FRG) [8], and an antiserum against 6-keto-PGFl, was raised in rabbits as described previously [9]. 3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) was from Sigma (St. Louis, MO).…”

Section: Reagentsmentioning

confidence: 99%

“…PGI 2 (in the form of the stable metabolite 6-keto-PGF~) and LTC 4 were determined radioimmunologically as described previously [8,9]. Aliquots of the supernates were mixed with [3H]-labelled 6-keto-PGFl~ or LTC4, respectively and a rabbit antiserum (6-keto-PGFl~) or a monoclonal antibody (LTC4).…”

Section: Quantification Of Pgi 2 and Ltc 4 In The Supernates Of Macromentioning

confidence: 99%

Suppression of endotoxin mitogenicity of spleen cells by lipoxygenase inhibitors and its reversal by 13-hydroxyoctadecadienoic acid

Elekes¹,

Jakobs²,

Schade³

1993

FEMS Immunology &Amp; Medical Microbiology

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Abstract:The effects of several inhibitors of lipoxygenases were investigated in murine spleen cell cultures activated with endotoxin (lipopolysaccharide) It was found that these inhibitors interfere with the proliferative response of the cultures. Indomethacin, a specific cyclooxygenase inhibitor, had no such effect. Endotoxin induced the synthesis of tumour necrosis factor a in spleen cells which was prevented by treatment with a lipoxygenase inhibitor. The inhibition of the mitogenic effect of endotoxin could be reversed by addition of 13-hydroxyoctadecadienoic acid. This was not the case with leukotriene B 4 and C 4 or 15-hydroxyeicosatetraenoic acid. In contrast, these substances had inhibitory effects on the mitogenicity of spleen cells. It is suggested that 13-hydroxyoctadecadienoic acid is involved in the development of the mitogenic reaction, possibly on the level of tumour necrosis factor a production of macrophages present in the cultures.

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A monoclonal antibody against the sulfidopeptide leukotrienes LTC4, LTD4 and LTE4

Cited by 17 publications

References 13 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

Case Report. Monascus purpureus—a new fungus of allergologic relevance

Suppression of endotoxin mitogenicity of spleen cells by lipoxygenase inhibitors and its reversal by 13-hydroxyoctadecadienoic acid

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