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Histamine Release (histamine + release)
Terms modified by Histamine Release Selected AbstractsCharacterization of Histamine Release Induced by Fluoroquinolone Antibacterial Agents In-vivo and In-vitroJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 5 2000KAZUHIKO MORI Characterization of histamine release induced by fluoroquinolone antibacterial agents, levofloxacin and ciprofloxacin, was investigated in-vivo and in-vitro. Intravenous injection of levofloxacin and ciprofloxacin at 1,10 mg kg,1 produced dose-related elevations in plasma histamine level in anaesthetized dogs. In contrast, levofloxacin was devoid of plasma histamine increment in anaesthetized rats at 100 mg kg,1, whereas ciprofloxacin at the same dose caused endogenous histamine release. Levofloxacin and ciprofloxacin induced non-cytotoxic secretion of histamine from all mast cells tested in a concentration-dependent manner, whereas rat skin and peritoneal mast cells were thirty- to one-hundred-times less sensitive to the effect of fluoroquinolones as compared with the canine skin mast cells. These results suggest that the functional heterogeneity of mast cells from different species in histamine releasing activity of fluoroquinolones may exist, and that mast cells from the dog appear to be particularly sensitive to the effect of the fluoroquinolones. [source] Effects of Low Power Laser Irradiation on Intracellular Calcium and Histamine Release in RBL-2H3 Mast CellsPHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 4 2007Wen-Zhong Yang Although laser irradiation has been reported to promote skin wound healing, the mechanism is still unclear. As mast cells are found to accumulate at the site of skin wounds we hypothesized that mast cells might be involved in the biological effects of laser irradiation. In this work the mast cells, RBL-2H3, were used in vitro to investigate the effects of laser irradiation on cellular responses. After laser irradiation, the amount of intracellular calcium ([Ca2+]i) was increased, followed by histamine release, as measured by confocal fluorescence microscopy with Fluo-3/AM staining and a fluorescence spectrometer with o -phthalaldehyde staining, respectively. The histamine release was mediated by the increment of [Ca2+]i from the influx of the extracellular buffer solution through the cation channel protein, transient receptor potential vanilloid 4 (TRPV4). The TRPV4 inhibitor, Ruthenium Red (RR) can effectively block such histamine release, indicating that TRPV4 was the key factor responding to laser irradiation. These induced responses of mast cells may provide an explanation for the biological effects of laser irradiation on promoting wound healing, as histamine is known to have multi-functions on accelerating wound healing. [source] Potentiation of Histamine Release by Microfungal (1,3)- and (1,6)-,-D-GlucansBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 6 2007Peter Holck The mechanisms by which they induce these effects are, however, not clear. In the present study, mediator release and its potentiation by the (1,3)-,-D-glucan as well as by the (1,6)-,-D-glucan found in yeast and other fungi were therefore examined. Blood leucocytes from healthy volunteers and from patients allergic to house dust mite were incubated with (1,3)-,-D-glucans with increasing 1,6-branchings: curdlan [a linear (1,3)-,-D-glucan], laminarin and scleroglucan, and furthermore with pustulan, a linear (1,6)-,-D-glucan. Histamine release was not observed on exposure to the glucans only, but in the presence of anti-immunoglobulin E (IgE) antibody or specific antigens, all the glucans investigated led to an enhancement of the IgE-mediated histamine release. The glucans induced a significant potentiation of the mediator release when present at concentrations in the range of 2,5 × 10,5 M. These results suggest that (1,3)-,-D-glucan as well as (1,6)-,-D-glucan aggravates IgE-mediated histamine release. Knowledge concerning the effects of glucans on immune responses may be of importance for understanding and treating inflammatory and allergic diseases. [source] Gastro-duodenal digestion products of the major peanut allergen Ara h 1 retain an allergenic potentialCLINICAL & EXPERIMENTAL ALLERGY, Issue 10 2006T. Eiwegger Summary Background The process of gastro-duodenal digestion may play a role in determining the allergenic properties of food proteins. The sensitizing and allergenic potential of digestion products of highly degraded allergens, such as the major peanut allergen Ara h 1, is currently under debate. We evaluated the effect of in vitro gastro-duodenal digestion of Ara h 1 on T cell reactivity and basophil histamine release. Methods An in vitro model of gastro-duodenal digestion was used to investigate changes in the allergenic properties of Ara h 1 using in vitro assays monitoring T cell reactivity (proliferation, cytokine production) and histamine release of basophils from peanut allergic individuals. The digestion process was monitored using an SDS-PAGE gel. Results In vitro gastric digestion led to rapid degradation of Ara h 1 into small fragments Mr L5600. Gastric digestion did not affect the ability of Ara h 1 to stimulate cellular proliferation. Gastro-duodenal digestion significantly reduced its ability to stimulate clonal expansion (P<0,05; Wilxocon's signed rank test). The Th-2 type cytokine polarization of T cells from peanut allergic donors (IFN-,/IL-13 ratio and IFN-,/IL-4 ratio of CFSElow CD4+ T cells) remained unchanged regardless of the level of digestion. Histamine release of basophils from peanut allergic individuals was induced to the same extent by native Ara h 1 and its digestion products. Conclusion Gastro-duodenal digestion fragments of Ara h 1 retain T cell stimulatory and IgE-binding and cross-linking properties of the intact protein. [source] Potato lectin activates basophils and mast cells of atopic subjects by its interaction with core chitobiose of cell-bound non-specific immunoglobulin ECLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2007S. N. Pramod Summary A major factor in non-allergic food hypersensitivity could be the interaction of dietary lectins with mast cells and basophils. Because immunoglobulin E (IgE) contains 10,12% carbohydrates, lectins can activate and degranulate these cells by cross-linking the glycans of cell-bound IgE. The present objective focuses on the effect of potato lectin (Solanum tuberosum agglutinin; STA) for its ability to release histamine from basophils in vitro and mast cells in vivo from non-atopic and atopic subjects. In this study, subjects were selected randomly based on case history and skin prick test responses with food, pollen and house dust mite extracts. Skin prick test (SPT) was performed with STA at 100 µg/ml concentration. Histamine release was performed using leucocytes from non-atopic and atopic subjects and rat peritoneal exudate cells. SPT on 110 atopic subjects using STA showed 39 subjects positive (35%); however, none showed STA-specific IgE; among 20 non-atopic subjects, none were positive by SPT. Maximal histamine release was found to be 65% in atopic subjects (n = 7) compared to 28% in non-atopic subjects (n = 5); the release was inhibited specifically by oligomers of N -acetylglucosamine and correlates well with serum total IgE levels (R2 = 0·923). Binding of STA to N -linked glycoproteins (horseradish peroxidase, avidin and IgG) was positive by dot blot and binding assay. As potato lectin activates and degranulates both mast cells and basophils by interacting with the chitobiose core of IgE glycans, higher intake of potato may increase the clinical symptoms as a result of non-allergic food hypersensitivity in atopic subjects. [source] Involvement of hypoxia-inducible factor-1 HiF(1,) in IgE-mediated primary human basophil responsesEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 12 2009Vadim V. Sumbayev Abstract Basophils play a pivotal role in regulating chronic allergic inflammation as well as angiogenesis. Here, we show for the first time that IgE-mediated activation of primary human basophils results in protein accumulation of the ,-subunit of hypoxia-inducible factor 1, (HIF-1,), which is differentially regulated compared with signals controlling histamine release. HIF-1 facilitates cellular adaptation to hypoxic conditions such as inflammation and tumour growth by controlling glycolysis, angiogenesis and cell adhesion. ERK and p38 MAPK, but not reactive oxygen species (ROS), ASK1 or PI 3-kinase, were critical for IgE-mediated accumulation of HIF-1,, although the latter crucially affected degranulation. Abrogating HIF-1, expression in basophils using siRNA demonstrated that this protein is essential for vascular endothelial growth factor (VEGF) mRNA expression and, consequently, release of VEGF protein. In addition, HIF-1, protein alters IgE-induced ATP depletion in basophils, thus also supporting the production of the pro-allergic cytokine IL-4. [source] Mast cell lines HMC-1 and LAD2 in comparison with mature human skin mast cells , drastically reduced levels of tryptase and chymase in mast cell linesEXPERIMENTAL DERMATOLOGY, Issue 9 2010Sven Guhl Please cite this paper as: Mast cell lines HMC-1 and LAD2 in comparison with mature human skin mast cells , drastically reduced levels of tryptase and chymase in mast cell lines. Experimental Dermatology 2010; 19: 845,847. Abstract:, To circumvent the costly isolation procedure associated with tissue mast cells (MC), two human MC lines, i.e. HMC-1 and LAD2, are frequently employed, but their relation to mature MC is unknown. Here, we quantitatively assessed their expression of MC markers in direct comparison to skin MC (sMC). sMC expressed all lineage markers at highest and HMC-1 cells at lowest levels. LAD2 cells expressed comparable high-affinity IgE receptor , (Fc,RI,) and Fc,RI, but less Fc,RI, than sMC and displayed slightly reduced, but robust Fc,RI-mediated histamine release. Only minor differences were found for total histamine content and c-Kit expression. Huge, and to this level unexpected, differences were found for MC tryptase and chymase, with sMC >>> LAD2 > HMC-1. Taken together, HMC-1 cells represent very immature malignantly transformed MC, whereas LAD2 cells can be considered intermediately differentiated. Because of the minute levels of MC proteases, MC lines can serve as surrogates of tissue MC to a limited degree only. [source] Semi-purification of the immunoglobulin E-sweat antigen acting on mast cells and basophils in atopic dermatitisEXPERIMENTAL DERMATOLOGY, Issue 4 2006A. Tanaka Background:, Sweating aggravates the symptoms of atopic dermatitis (AD). We have recently reported positive skin reactions and histamine release from basophils in response to autologous sweat in patients with AD. Objective:, To characterize the biochemical and immunological properties of the substance in sweat that evokes histamine release and to study the usability of the basophil-histamine release test with the sweat antigen for AD. Methods:, Sweat collected from healthy volunteers was purified using chromatographies. Serum immunoglobulin (Ig)E of four patients with AD were purified using an affinity-chromatography column with anti-IgE antibodies. The amount of semi-purified sweat antigen (138 ng protein/ml) that induced a half-maximum reaction of basophils of a patient with AD was utilized for the basophil histamine release test. The involvement of specific IgE and high-affinity IgE receptor (Fc,RI) in the reactions was examined using basophils of healthy volunteers, a human mast cell line (LAD2), and a rat basophilic leukemia cell line transfected with human ,-subunit of Fc,RI (RBL-48). Results:, The semi-purified sweat antigen induced histamine release from the basophils of 47 of 61 (74.6%) patients with AD and four of 46 (8.7%) healthy controls. Both basophils and mast cells sensitized with the patient-derived IgE showed degranulation upon stimulation with the sweat antigen. However, no reaction was observed when cells were sensitized with myeloma IgE or the antigen was treated with proteases. Conclusion:, The semi-purified standardized sweat antigen consists of a protein that induces degranulation of basophils and mast cells via antigen-specific IgE and Fc,RI in patients with AD. [source] Pathophysiology of pruritus in atopic dermatitis: an overviewEXPERIMENTAL DERMATOLOGY, Issue 1 2002Sonja Ständer Abstract: Pruritus is an essential feature of atopic dermatitis (AD) and the diagnosis of active AD cannot be made without the history of itching. Because of the high impact on life quality, most of the patients measure the severity of eczema by the intensity of pruritus rather than appearance of skin lesions. However, although pruritus is a cardinal symptom of AD, its mechanism and association with the cutaneous nervous system is not completely understood. Recently, a considerable progress has been achieved in clarifying the complex pathophysiology of pruritus in AD. As a cutaneous sensory perception, itch requires excitation of neuropeptide-containing free nerve endings of unmyelinated nociceptor fibers. It is well known that histamine and acetylcholine provoke itch by direct binding to ,itch receptors' and several mediators such as neuropeptides, proteases or cytokines indirectly via histamine release. Interestingly, some variations of these complex mechanisms could be demonstrated in patients with AD. This review highlights the recent knowledge of different mechanisms which may be involved in regulating pruritus in patients with AD potentially leading to new therapeutic applications for the treatment of itch in AD. [source] Studies on the association between immunoglobulin E autoreactivity and immunoglobulin E-dependent histamine-releasing factorsIMMUNOLOGY, Issue 2 2002Ilona Kleine Budde Summary It has been reported that serum immunoglobulin E (IgE) from certain atopic patients can sensitize basophils to release histamine in response to IgE-dependent histamine-releasing factors (HRFs). It has also been shown that patients suffering from severe forms of atopy may contain IgE autoantibodies. It was investigated whether HRF-responsive sera contained IgE autoantibodies and if there was an association between IgE autoreactivity and IgE-dependent responsiveness to HRF. The presence of HRF-responsive IgE (IgE+) in serum of patients with respiratory atopy was determined by stimulating stripped human basophils sensitized by serum with peripheral blood mononuclear cell (PBMC)-derived HRF, and measuring the release of histamine. In parallel, these sera were screened for the presence of IgE autoantibodies to nitrocellulose-blotted human cellular extracts. The capacity of IgE autoantigen-containing preparations to induce histamine release was tested in the stripped basophil assay. Eleven out of 52 sera contained IgE autoantibodies to blotted cellular extracts of human PBMCs or of the human epithelial cell line A431. No significant association was found between IgE autoreactivity and IgE-dependent responsiveness to HRF: 7/26 IgE+ sera contained IgE to human cellular extracts, and 4/26 of the sera without IgE+ did also. IgE autoantigen-containing extracts did not induce histamine release of appropriately sensitized basophils. By size-exclusion chromatography it was shown that a 32,000 MW autoantigen eluted in the >55,000 MW fraction, which indicates that this protein forms polymers or complexes with other macromolecules. This might explain the discrepancy between binding and histamine-releasing activity. A 20,000 MW IgE-defined autoantigen cross-reacted with a shrimp allergen. Our results indicate that IgE-reactivity to immunoblotted human protein and IgE-dependent HRF activity are distinct entities that may co-occur in atopic patients. [source] Naturally occurring polyphenolic antioxidants modulate IgE-mediated mast cell activationIMMUNOLOGY, Issue 4 2000S.-S. Chen Summary Reactive oxygen species (ROS) are known to modulate activities of a host of kinases, phosphatases and transcription factors. Rutin and chlorogenic acid (CGA) are the major polyphenolic antioxidants present in the small molecular fraction of smokeless tobacco leaf extracts, as ascertained by reverse-phase high-pressure liquid chromatography (HPLC) and mass spectrometry. Levels of intracellular ROS in resting versus antigen,immunoglobulin E (IgE)-challenged murine mast cells were measured at 510 nm by fluorescence-activated cell sorting (FACS) using carboxy-dichlorofluorescein (DCFH-DA). Enhanced ROS production was observed in IgE-sensitized mast cells following antigenic challenge. Rutin and CGA reduced ROS levels in antigen,IgE-activated mast cells. Concomitantly, they also profoundly inhibited histamine release by these activated mast cells. In contrast, rutin and CGA augmented the inducible cytokine messages, i.e. interleukin (IL)-10, IL-13, interferon-, (IFN-,), IL-6 and tumour necrosis factor-, (TNF-,) in IgE-sensitized mast cells following antigen challenge. This study indicates that tobacco polyphenolic antioxidants that quench intracellular ROS, differentially affect two effector functions of antigen,IgE-activated mast cells. This model system may be employed to determine the molecular target of polyphenols. The potential role of these polyphenolic antioxidants on IgE-mediated allergy in vivo depends on a balance of their differential effects on mast cell activation. [source] Consequences of eicosapentaenoic acid (n-3) and arachidonic acid (n-6) supplementation on mast cell mediatorsJOURNAL OF ANIMAL PHYSIOLOGY AND NUTRITION, Issue 7-8 2004T. Gueck Summary Mast cells are important players in the pathogenesis of atopic diseases. These cells release immediate-phase and late-phase mediators of inflammation. Fatty acids are incorporated in cellular membranes and therefore seem to influence mediator production and release. A study was conducted to assess the effects of eicosapentaenoic acid (EPA, 20:5n-3) and arachidonic acid (AA, 20:4n-6) on mast cell mediators in a canine mastocytoma cell line (C2). Cells were cultured in a basic medium (Dulbecco's modified Eagle's medium/HAM's F12 1 : 1, DEH), DEH supplemented with 14.0 ,m EPA (DEH-EPA) or 14 ,m AA (DEH-AA). The DEH-AA cultured cells had increased spontaneous and mastoparan-stimulated PGE2 production and histamine release. Furthermore, the tryptase activity was increased. The DEH-EPA cultured cells rendered elevated levels of PGE2 and histamine release compared with DEH only after stimulation. These levels were significantly lower in comparison to DEH-AA. The increased PGE2 production of C2 cultured in DEH-AA is the consequence of the AA enrichment, because AA is the precursor of PGE2. However, the different effects by AA and EPA on mast cell mediators possibly reflect the higher susceptibility of long chain polyunsaturated fatty acids (PUFA) to undergo lipid peroxidation, because it is known that altered cellular redox state influences mediator production and release. [source] Mechanisms of cytoprotective effect of amino acids on local toxicity caused by sodium laurate, a drug absorption enhancer, in intestinal epitheliumJOURNAL OF PHARMACEUTICAL SCIENCES, Issue 3 2002Yoko Endo Abstract Several amino acids, including L -glutamine (L -Gln), were found to protect the intestinal epithelial cells from the local toxicity caused by a drug absorption enhancer, sodium laurate (C12), in our previous study. To develop more efficient and safer formulations for enhancing drug absorption, the mechanisms of cytoprotection by amino acids were studied using rats and Caco-2 cells. Four amino acids, including L -Gln, could generally maintain the absorption-promoting action of C12, although taurine tended to attenuate it. Three amino acids, except for L -Gln, significantly suppressed the decrease in the transepithelial electrical resistance caused by C12. Quercetin, an inhibitor for biosynthesis of heat shock protein 70 (HSP70), masked only the protective effect of L -Gln in both rat large intestine and Caco-2 cells. Western blot analysis indicated clearly that HSP70 is induced extensively only by the addition of L -Gln in both rat large-intestinal cells and Caco-2 cells. C12 was found to increase the intracellular concentration of Ca2+ ([Ca2+]i) remarkably, and amino acids, especially L -arginine, L -methionine, and taurine, significantly attenuated the increase in [Ca2+]i caused by C12. Furthermore, although C12 stimulated the release of histamine, an inflammatory mediator, from rat large-intestinal tissue, amino acids were also found to suppress the release of histamine enhanced by C12. The results in the present study showed that an induction of HSP70, a decrease in [Ca2+]i elevated by C12, and a suppression of histamine release stimulated by C12 should be involved in the mechanisms behind the cytoprotective action of amino acids against the local toxicity caused by C12. © 2002 Wiley-Liss, Inc. and the American Pharmaceutical Association J Pharm Sci 91:730,743, 2002 [source] Anti-allergic properties of Mangifera indica L. extract (Vimang) and contribution of its glucosylxanthone mangiferinJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 3 2006Dagmar Garcķa Rivera Vimang is the brand name of formulations containing an extract of Mangifera indica L., ethnopharmacologically used in Cuba for the treatment of some immunopathological disorders, including bronchial asthma, atopic dermatitis and other allergic diseases. However, the effects of Vimang on allergic response have not been reported until now. In this study, the effects of Vimang and mangiferin, a C-glucosylxanthone isolated from the extract, on different parameters of allergic response are reported. Vimang and mangiferin showed a significant dose-dependent inhibition of IgE production in mice and anaphylaxis reaction in rats, histamine-induced vascular permeability and the histamine release induced by compound 48/80 from rat mast cells, and of lymphocyte proliferative response as evidence of the reduction of the amount of B and T lymphocytes able to contribute to allergic response. In these experiments, ketotifen, promethazine and disodium cromoglicate were used as reference drugs. Furthermore, we demonstrated that Vimang had an effect on an in-vivo model of inflammatory allergy mediated by mast cells. These results constitute the first report of the anti-allergic properties of Vimang on allergic models, as well as suggesting that this natural extract could be successfully used in the treatment of allergic disorders. Mangiferin, the major compound of Vimang, contributes to the anti-allergic effects of the extract. [source] Phytochemical analysis and anti-allergic study of Agave intermixta Trel. and Cissus sicyoides L.JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 9 2004A. M. Quķlez Agave intermixta Trel. (Maguey) and Cissus sicyoides L. (Bejuco caro) are Caribbean plant species from the Dominican Republic used locally in traditional popular medicine that have shown an anti-inflammatory effect in experimental animal models. A phytochemical analysis on these species allowed us the isolation and identification of the steroidal sapogenins hecogenin and diosgenin from Maguey and the hydroxystilbene resveratrol from Bejuco caro. The effects of these plant extracts and their isolated constituents on compound-48/80-induced histamine release from peritoneal mast cells were investigated. Significant inhibition was produced by 0.5 mg mL,1 of a methanolic extract of Bejuco (41.1%) and by its constituent resveratrol (82.4%) at a dose of 250 ,M. However, none of the steroidal sapogenins from A. intermixta showed a significant inhibitory effect on histamine release from mast cells. From these results, it can be deduced that the in-vitro anti-allergic activity towards the release of histamine from mast cells shown by the methanolic extract of C. sicyoides may be mediated by its constituent resveratrol and might contribute to the anti-inflammatory activity shown by this species. [source] Characterization of Histamine Release Induced by Fluoroquinolone Antibacterial Agents In-vivo and In-vitroJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 5 2000KAZUHIKO MORI Characterization of histamine release induced by fluoroquinolone antibacterial agents, levofloxacin and ciprofloxacin, was investigated in-vivo and in-vitro. Intravenous injection of levofloxacin and ciprofloxacin at 1,10 mg kg,1 produced dose-related elevations in plasma histamine level in anaesthetized dogs. In contrast, levofloxacin was devoid of plasma histamine increment in anaesthetized rats at 100 mg kg,1, whereas ciprofloxacin at the same dose caused endogenous histamine release. Levofloxacin and ciprofloxacin induced non-cytotoxic secretion of histamine from all mast cells tested in a concentration-dependent manner, whereas rat skin and peritoneal mast cells were thirty- to one-hundred-times less sensitive to the effect of fluoroquinolones as compared with the canine skin mast cells. These results suggest that the functional heterogeneity of mast cells from different species in histamine releasing activity of fluoroquinolones may exist, and that mast cells from the dog appear to be particularly sensitive to the effect of the fluoroquinolones. [source] The development of a suitable manufacturing process for ,Benifuuki' green tea beverage with anti-allergic effectsJOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE, Issue 10 2005Hiroshi Nagai Abstract Epigallocatechin-3- O -(3- O -methyl) gallate (EGCG3,Me) has been reported to inhibit type I allergy better than epigallocatechin gallate (EGCG), a major catechin in tea leaves (Camellia sinensis L). We examined the effects of extraction and sterilization on the catechin content and histamine release from mast cells, as a representative reaction of early phase allergy, in the manufacture of ,Benifuuki' green tea beverage. Among various varieties of tea, the cultivar ,Benifuuki' contains approximately 2% of EGCG3,Me. Ester-type catechins and their epimers increased with the increased extraction temperature of the tea. A tea infusion, extracted at 90 °C, strongly inhibited histamine release from mast cells. Furthermore, sterilization affected the catechin content in the manufactured green tea beverage. Sterilization at high temperature promoted the isomerization of catechins and the sterilized green tea beverage had a strong inhibitory effect. When EGCG3,Me, EGCG, epicatechin-3- O -gallate (ECG) and their epimers, GCG3,Me (gallocatechin-3- O -(3- O -methyl) gallate), GCG (gallocatechin-3- O -gallate) and CG (catechin-3- O -gallate) were compared, the anti-allergic effect of GCG3,Me was strongest, and the order of activity was GCG3,Me > EGCG3,Me > GCG > EGCG. We consequently suggest that it was necessary to extract components from tea at the highest temperature possible, and to pasteurize under retort conditions (118.1 °C, 20 min), to manufacture functional green tea beverage with an anti-allergic action. Copyright © 2005 Society of Chemical Industry [source] Cigarette smoke facilitates allergen penetration across respiratory epitheliumALLERGY, Issue 3 2009K. Gangl Background:, The association between cigarette smoke exposure and allergic airway disease is a matter for debate. We sought to investigate in an in vitro system whether active smoking reduces the integrity and barrier function of the respiratory epithelium and thus facilitates allergen penetration. Methods:, We cultured the human bronchial epithelial cell line 16HBE14o, in a transwell culture system as a surrogate for the intact respiratory epithelium. The cell monolayer was exposed to standardized cigarette smoke extract (CSE). The extent and effects of trans-epithelial allergen penetration were measured using 125I-labelled purified major respiratory allergens (rBet v 1, rPhl p 5 and rDer p 2) and histamine release experiments. Results:, Exposure of cells to concentrations of CSE similar to those found in smokers induced the development of para-cellular gaps and a decrease in trans-epithelial resistance. CSE exposure induced a more than threefold increase in allergen penetration. Increased subepithelial allergen concentrations provoked a substantial augmentation of histamine release from sensitized basophils. Conclusions:, Our results indicate that cigarette smoke is a potent factor capable of reducing the barrier function of the respiratory epithelium for allergens and may contribute to increased allergic inflammation, exacerbation of allergic disease and boosting of IgE memory. [source] Gender difference, sex hormones, and immediate type hypersensitivity reactionsALLERGY, Issue 11 2008W. Chen Gender differences in the development and prevalence of human diseases have long been recognized. Immense interest grows in the understanding of the role of sex hormones in the homeostasis of immunity. Asthma predominates in boys before puberty and this gender preference reverses after puberty and in adulthood, when adult women tend to have a more severe disease, often recalcitrant to treatment. Atopic eczema in preschool children shows insignificant gender difference or male preponderance in different studies, with more adult females suffering from atopic eczema. The limited data on the prevalence of immediate hypersensitivity to hymenoptera venom show controversial results. Discrepancy exists regarding the gender difference in food allergy, with females reporting significantly more allergic reactions in questionnaire studies. In general, adverse reactions to nonionic iodinated radiocontrast media are more commonly observed in females. The course of allergic diseases varies unpredictably during pregnancy, whereas hormone replacement therapy in postmenopausal women usually has a favorable influence on the course of asthma. Experiments in rodents confirm an effect of estrogens on mast cell activation and allergic sensitization, while progesterone is shown to suppress histamine release but potentiate IgE induction. Dehydroepiandrosterone may antagonize the production of Th2 cytokines but the effect of testosterone and the other androgens remains less defined. Actual data from human studies are lacking. [source] The effect of multiple allergens on histamine release in vivo assessed by skin prick testALLERGY, Issue 11 2008G. Liccardi No abstract is available for this article. [source] Human mast cells express receptors for IL-3, IL-5 and GM-CSF; a partial map of receptors on human mast cells cultured in vitroALLERGY, Issue 10 2004C. Dahl Background:, Mast cells have long been recognized as the principal cell type that initiates the inflammatory response characteristic of acute allergic type 1 reactions. Our goal has been to further characterize maturation of progenitors to mast cells. Methods:, Mast cells were cultured from human cord blood derived CD133+ progenitors. Mast cell function was tested using histamine release. During differentiation mast cells surface marker expression was monitored by flow cytometry. Results:, CD133+ progenitors expressed the early haematopoietic and myeloid lineage markers CD34, CD117, CD13 and CD33. Mature mast cells expressed CD117, CD13 and CD33, and expression of the high affinity immunoglobulin E recpetor Fc,RI increased during culture. Cytokine receptors interleukin (IL)-5R, IL-3R, granulocyte-macrophage-colony stimulating factor (GM-CSF)R and IL-18R were expressed at high levels during maturation. Chemokine receptors CXCR4 and CXCR2 were highly expressed on both newly purified CD133+ cells and mature cells. Conclusion:, Human mast cells can be cultured from a CD34+/CD117+/CD13+/CD33+ progenitor cell population in cord blood that is tryptase and chymase negative. Developing and mature mast cells express a wide range of chemokine and cytokine receptors. We found high levels of expression of CD123, IL-5R and GM-CSF receptors, also found on eosinophils and basophils, and high levels of expression of the receptor for the inflammatory cytokine IL-18. [source] Tomato profilin Lyc e 1: IgE cross-reactivity and allergenic potencyALLERGY, Issue 5 2004S. Westphal Background:, To date, very little data are available about the nature of tomato allergens. Immunoglobulin E (IgE) cross-reactive profilins have been suggested to account for allergic symptoms in patients suffering from tomato allergy. Methods:, The cDNA of tomato profilin was amplified by reversely transcribed polymerase chain reaction (RT-PCR) from total RNA extracted from ripe tomato fruit. The gene was cloned into the pET101D expression plasmid and the protein was produced in Escherichia coli BL21. Purification was performed via poly- l -proline (PLP) affinity chromatography. IgE reactivity of recombinant tomato profilin was investigated by immunoblot and enzyme-linked immunosorbent assay. IgE-inhibition studies were performed to analyse cross-reactivity with other profilins. To determine the allergenic activity of the recombinant protein, basophil histamine release assays using sera of patients with adverse reactions to tomato were performed. Results:, Profilin was identified as a new minor allergen in tomato fruits. The recombinant tomato profilin comprises 131 amino acids and high sequence identity to other allergenic food and pollen profilins. It was shown to be IgE-reactive with a prevalence of 22% (11/50) in tomato-allergic patients. In patients with tomato allergy and multiple sensitization to other foods and birch pollen, IgE directed against tomato profilin showed a strong cross-reactivity with profilins from plant food sources and birch pollen. The tomato profilin was able to induce mediator release from human basophils. Conclusion:, The tomato profilin is a minor allergen in tomato fruit. Thus, it shows biological activity, as confirmed by in vitro histamine release assays with human basophils and thereby has the potential to account for clinical symptoms in tomato-allergic patients. [source] Effects of Low Power Laser Irradiation on Intracellular Calcium and Histamine Release in RBL-2H3 Mast CellsPHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 4 2007Wen-Zhong Yang Although laser irradiation has been reported to promote skin wound healing, the mechanism is still unclear. As mast cells are found to accumulate at the site of skin wounds we hypothesized that mast cells might be involved in the biological effects of laser irradiation. In this work the mast cells, RBL-2H3, were used in vitro to investigate the effects of laser irradiation on cellular responses. After laser irradiation, the amount of intracellular calcium ([Ca2+]i) was increased, followed by histamine release, as measured by confocal fluorescence microscopy with Fluo-3/AM staining and a fluorescence spectrometer with o -phthalaldehyde staining, respectively. The histamine release was mediated by the increment of [Ca2+]i from the influx of the extracellular buffer solution through the cation channel protein, transient receptor potential vanilloid 4 (TRPV4). The TRPV4 inhibitor, Ruthenium Red (RR) can effectively block such histamine release, indicating that TRPV4 was the key factor responding to laser irradiation. These induced responses of mast cells may provide an explanation for the biological effects of laser irradiation on promoting wound healing, as histamine is known to have multi-functions on accelerating wound healing. [source] Phlomis umbrosa root inhibits mast cell-dependent allergic reactions and inflammatory cytokine secretionPHYTOTHERAPY RESEARCH, Issue 2 2008Tae-Yong Shin Abstract The effect of an aqueous extract of Phlomis umbrosa Turcz. (Labiatae) root (PUAE) on mast cell-dependent allergic reactions and inflammatory cytokine secretion were investigated. PUAE (0.01,1 g/kg) inhibited compound 48/80-induced systemic allergic reaction. When PUAE was employed in a systemic allergic reaction test, the plasma histamine levels were reduced in a dose-dependent manner. PUAE (0.1 and 1 g/kg) also significantly inhibited the local allergic reaction activated by anti-dinitrophenyl (DNP) IgE. PUAE (0.001,1 mg/mL) dose-dependently inhibited the histamine release from rat peritoneal mast cells activated by compound 48/80 or anti-DNP IgE. PUAE (0.01,1 mg/mL) inhibited the secretion of interleukin (IL)-1, in phorbol 12-myristate 13-acetate plus calcium ionophore A23187-stimulated human mast cell line (HMC-1) cells. PUAE (1 mg/mL) inhibited the gene expression and production of the main inflammatory cytokine, TNF- ,, in HMC-1 cells. These results provide evidence that PUAE may be beneficial in the treatment of allergic diseases. Copyright © 2007 John Wiley & Sons, Ltd. [source] Action of,,Rubus coreanus extract on systemic and local anaphylaxisPHYTOTHERAPY RESEARCH, Issue 6 2002Tae-Yong Shin Abstract The effect was investigated of the aqueous extract of Rubus coreanus Miq. (Rosaceae) fruits (RCAE) on systemic and local anaphylaxis. RCAE (0.01,1,g/kg) dose-dependently inhibited systemic anaphylaxis induced by compound 48/80 in mice. RCAE (1,g/kg) also significantly inhibited local anaphylaxis activated by anti-DNP IgE. Pretreatment with RCAE at the same concentration before systemic anaphylaxis reduced the plasma histamine levels in a dose-dependent manner. RCAE (0.001,1,mg/mL) dose-dependently inhibited the histamine release from rat peritoneal mast cells (RPMC) activated by compound 48/80 or anti-DNP IgE. The level of cAMP in RPMC, when RCAE was added, significantly increased, compared with that of the normal control. Moreover, RCAE,(0.01,1,mg/mL) had a significant inhibitory effect on anti-DNP IgE-induced tumour necrosis factor-, production from RPMC. These results indicate that RCAE may possess antianaphylactic action. Copyright © 2002 John Wiley & Sons, Ltd. [source] The undesirable effects of neuromuscular blocking drugsANAESTHESIA, Issue 2009C. Claudius Summary Neuromuscular blocking drugs are designed to bind to the nicotinic receptor at the neuromuscular junction. However, they also interact with other acetylcholine receptors in the body. Binding to these receptors causes adverse effects that vary with the specificity for the cholinergic receptor in question. Moreover, all neuromuscular blocking drugs may cause hypersensitivity reactions. Often the symptoms are mild and self-limiting but massive histamine release can cause systematic reactions with circulatory and respiratory symptoms and signs. At the end of anaesthesia, no residual effect of a neuromuscular blocking drug should be present. However, the huge variability in response to neuromuscular blocking drugs makes it impossible to predict which patient will suffer postoperative residual curarization. This article discusses the undesirable effects of the currently available neuromuscular blocking drugs including the definitions, diagnosis and causes of hypersensitivity reactions and postoperative residual curarisation. [source] Study on the antinociceptive action of Tyr-K-MIF-1, a peptide from the MIF familyAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 2 2007R. Zamfirova Summary 1 Tyr-K-MIF-1 is a melanocyte inhibiting factor (MIF) neuropeptide, isolated from the brain. Opposite to other MIFs (Tyr-MIF-1, Tyr-W-MIF-1), it has a very low affinity for opiate , -receptors, but interacts with Tyr-MIF-1 specific binding sites. Tyr-MIF-1 and Tyr-W-MIF-1 evoke antinociception mainly by activating opioid receptors. We investigated the possible antinociceptive effect of Tyr-K-MIF-1 and the involvement of histaminergic system in its mechanism of action. 2 Tested on rats by paw-pressure test, Tyr-K-MIF-1 (0.5, 1 and 2 mg kg,1) was associated with short-lasting analgesia, which was abolished by naloxone (1 mg kg,1). 3 Injected intraperitoneally (i.p.) 15 min before Tyr-K-MIF-1, antagonists of H1 (diphenhydramine, 100 mg kg,1) or H2 (famotidine, 0.3 and 0.6 mg kg,1) histamine receptors diminished peptide antinociceptive effect. Simultaneous H1 - and H2 blockade, as well as pretreatment with 5 mg kg,1 dimaprit (H2 agonist) abolished Tyr-K-MIF-1-induced analgesia. Tyr-K-MIF-1-induced analgesia was also abolished by treatment with R-(,)-methylhistamine (10 mg kg,1, i.p.), an H3 histamine receptor agonist that acts to inhibit histamine release. 4 Our results together with data reported in the literature support the conclusion that activation of the histaminergic system is involved in the mechanism of Tyr-K-MIF-1-induced antinociception. [source] Potentiation of Histamine Release by Microfungal (1,3)- and (1,6)-,-D-GlucansBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 6 2007Peter Holck The mechanisms by which they induce these effects are, however, not clear. In the present study, mediator release and its potentiation by the (1,3)-,-D-glucan as well as by the (1,6)-,-D-glucan found in yeast and other fungi were therefore examined. Blood leucocytes from healthy volunteers and from patients allergic to house dust mite were incubated with (1,3)-,-D-glucans with increasing 1,6-branchings: curdlan [a linear (1,3)-,-D-glucan], laminarin and scleroglucan, and furthermore with pustulan, a linear (1,6)-,-D-glucan. Histamine release was not observed on exposure to the glucans only, but in the presence of anti-immunoglobulin E (IgE) antibody or specific antigens, all the glucans investigated led to an enhancement of the IgE-mediated histamine release. The glucans induced a significant potentiation of the mediator release when present at concentrations in the range of 2,5 × 10,5 M. These results suggest that (1,3)-,-D-glucan as well as (1,6)-,-D-glucan aggravates IgE-mediated histamine release. Knowledge concerning the effects of glucans on immune responses may be of importance for understanding and treating inflammatory and allergic diseases. [source] Sweat antigen induces histamine release from basophils of patients with cholinergic urticaria associated with atopic diathesisBRITISH JOURNAL OF DERMATOLOGY, Issue 2 2009S. Takahagi Summary Background, We previously demonstrated that the semipurified human sweat antigen causes skin reactions and histamine release from basophils via specific IgE in patients with atopic dermatitis (AD). Patients with cholinergic urticaria (ChU) also develop skin reactions and histamine release of basophils in response to autologous sweat. Objectives, To study whether or not patients with ChU share sensitivity for the sweat antigen with patients with AD and to study the clinical characteristics among patients with ChU and the relationship with histamine-release activity of basophils. Methods, The sweat antigen that induces histamine release from basophils of patients with AD was prepared by Con-A, anion-exchange and reverse-phase chromatography. Relationships between histamine-release activity against the sweat antigen and clinical features of patients with ChU were analysed. Results, Twenty-three of 35 patients with ChU showed > 5% net histamine release in response to the semipurified sweat antigen, whereas none of healthy controls did so. In patients with ChU, histamine release in response to semipurified sweat antigen significantly correlated with the level of serum IgE and eosinophil numbers in peripheral blood. Incidence of each atopic disease in patients with ChU tended to be higher than in the general Japanese population. When the patients were categorized according to their responses in the histamine release test, the positive group tended to show a higher incidence of AD and bronchial asthma compared with the negative group. Conclusions, ChU and AD may share hypersensitivity to common antigens in sweat. The sweat allergy and atopic diathesis are associated with each other. [source] The long-acting ,-adrenoceptor agonist, indacaterol, inhibits IgE-dependent responses of human lung mast cellsBRITISH JOURNAL OF PHARMACOLOGY, Issue 1 2009Anne-Marie Scola Background and purpose:, The long-acting ,2 -adrenoceptor agonist, indacaterol, has been developed as a bronchodilator for the therapeutic management of respiratory diseases. The aim of the present study was to determine whether indacaterol has any anti-inflammatory activity. To this end, the effects of indacaterol on human lung mast cell responses were investigated. Experimental approach:, The effects of indacaterol, and the alternative long-acting ,-agonists formoterol and salmeterol, were investigated on the IgE-dependent release and generation of histamine, cysteinyl-leukotrienes and prostaglandin D2 from human lung mast cells. Moreover, the extent to which long-term (24,72 h) incubation of mast cells with long-acting ,-agonists impaired the subsequent ability of ,-agonists to inhibit mast cell responses was assessed. Key results:, Indacaterol was as potent and as efficacious as the full agonist, isoprenaline (EC50, ,4 nmol·L,1), at inhibiting the IgE-dependent release of histamine from mast cells. Formoterol was a full agonist whereas salmeterol was a partial agonist as inhibitors of histamine release. All three long-acting ,-agonists were effective inhibitors of the IgE-dependent generation of cysteinyl-leukotrienes and prostaglandin D2. Long-term incubation of mast cells with long-acting ,-agonists led to a reduction in the subsequent ability of ,-agonists to stabilize mast cell responses. This tendency to induce functional desensitization was least evident for indacaterol. Conclusions and implications:, Indacaterol is an effective inhibitor of the release of mediators from human lung mast cells. This suggests that, as well as bronchodilation, mast cell stabilization may constitute an additional therapeutic benefit of indacaterol. [source] | ||||||||||||||||||||||||||||||||||