Specific inhibition of immunoglobulin E‐mediated allergic reaction using antisense FcεRIα oligodeoxynucleotides

Kim, H M; Kim, K S; Lee, E H

doi:10.1046/j.1365-2567.1998.00453.x

Cited by 17 publications

(5 citation statements)

References 23 publications

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“…For example, in cultured neuronal cells, salicylate protects neurotoxicity elicited by the excitatory amino acid glutamate, 1 in cultured cardiac fibroblasts, it inhibits the inducible nitric oxide synthase, 2 in HeLa cells, it activates human heat‐shock transcription factor, 3 and in plants, it activates pathogenesis‐related genes in response to infection and injury 4 . 5 It is now well established that the mast cell triggers anaphylaxis in response to allergens by releasing chemical mediators 6 . Among the preformed and newly synthesized inflammatory substances released on degranulation of mast cells, histamine is the best characterized and most potent vasoactive mediator implicated in the acute phase of immediate‐type allergic reactions 7 .…”

Section: Introductionmentioning

confidence: 99%

Inhibition of mast cell‐dependent anaphylaxis by sodium salicylate

et al. 1999

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Sodium salicylate (NaSal) is a commonly used agent with a wide pharmacological spectrum. The objective of the present study was to investigate the effect of NaSal on anaphylaxis. NaSal (10-1 and 1 mm) significantly inhibited systemic anaphylaxis induced by compound 48/80 in rats. NaSal also significantly inhibited local anaphylaxis activated by anti-dinitrophenyl (DNP) immunoglobulin E (IgE). NaSal (10-1 and 1 mm) significantly inhibited histamine release from rat peritoneal mast cells (RPMC) activated by compound 48/80 or anti-DNP IgE. Northern-blot analysis demonstrated that a significantly reduced level of the mRNA of L-histidine decarboxylase was expressed in mast cells treated with NaSal, compared with that without NaSal. NaSal (10-2 and 10-1 mm) had a significant inhibitory effect on anti-DNP IgE-induced tumour necrosis factor-alpha secretion from RPMC. The level of cyclic AMP in RPMC, when NaSal (1 mm) was added, transiently and significantly increased about sixfold compared with that of basal cells. These results suggest a possible use of NaSal in managing mast cell-dependent anaphylaxis.

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Section: Introductionmentioning

confidence: 99%

Inhibition of mast cell‐dependent anaphylaxis by sodium salicylate

et al. 1999

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“…The control and LPS wells received the same amount of DMSO. The supernatants were then collected and assayed for TNF-a using mouse TNF-a ELISA kit as described previously (Kim et al, 1998).…”

Section: Methodsmentioning

confidence: 99%

Houttuynia cordata Thunb. Volatile Oil Exhibited Anti‐inflammatory Effects In Vivo and Inhibited Nitric Oxide and Tumor Necrosis Factor‐α Production in LPS‐stimulated Mouse Peritoneal Macrophages In Vitro

Liu

Fan

Zhang

et al. 2012

Phytotherapy Research

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Houttuynia cordata Thunb. (HC) is a medicinal herb that generally used in traditional Chinese medicine for treating allergic inflammation. The present study investigated the inhibitory effect of the volatile oil from HC Thunb. on animal models of inflammation and the production of inflammatory mediators in vivo and in vitro. In vivo, xylene-induced mouse ear edema, formaldehyde-induced paw edema and carrageenan-induced mice paw edema were significantly decreased by HC volatile oil. HC volatile oil showed pronounced inhibition of prostaglandin (PG) E2 and malondialdehyde production in the edematous exudates. In vitro exposure of mouse resident peritoneal macrophages to 1, 10, 100 and 1000 µg/mL of HC volatile oil significantly suppressed lipopolysaccharide (LPS)-stimulated production of NO and tumor necrosis factor-α (TNF-α) in a dose-dependent manner. Exposure to HC volatile oil had no effect on cell viability and systemic toxicity. Furthermore, HC volatile oil inhibited the production of NO and TNF-α by down-regulating LPS-stimulated iNOS and TNF-α mRNA expression. Western blot analysis showed that HC volatile oil attenuated LPS-stimulated synthesis of iNOS and TNF-α protein in the macrophages, in parallel. These findings add a novel aspect to the biological profile of HC and clarify its anti-inflammatory mechanism.

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“…Peritoneal macrophages (2.5 × 10 5 cells/well) were incubated with rIFN-␥ (20 U/ml), CT, rIFN-␥ plus LPS (10 g/ml) and rIFN-␥ plus various concentrations of CT for 24 h. Then the amount of TNF-␣ secreted by the cells was measured by a modified enzymelinked immunosorbent assay (ELISA), as described previously (Kim et al, 1998). The ELISA was devised by coating 96-well plates of murine monoclonal antibody with specificity for TNF-␣.…”

Section: Assay Of Tnf-˛releasementioning

confidence: 99%