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  • 1
    Electronic Resource
    Electronic Resource
    Effects of a cysteinyl leukotriene antagonist, ONO-1078 (pranlukast), on total airway resistance after antigen challenge in sensitized guinea pigs (1997)
    Springer
    Inflammation research 46 (1997), S. 143-146 
    Details
    ISSN: 1420-908X
    Keywords: Key words: Leukotriene — Allergic rhinitis — Guinea pig models — Total airway resistance — Nasal symptoms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Objective and Design: To define the role of leukotriene (LT) in allergic rhinitis, we examined the effects of a cysteinyl (Cys) LT antagonist (ONO-1078, pranlukast).¶Material: Actively sensitized Dunkin-Hartley guinea pigs.¶Treatment: ONO-1078 (pranlukast), 3–100 mg/kg p.o. l h before antigen challenge.¶Methods: Nasal symptoms (sneezing, nasal scratches), changes of total airway resistance (TAR by plethysmography) and eosinophil infiltration into the nasal mucosa were determined following topical antigen (OA) challenge. Dunnet's test (TAR and symptoms) and the Mann-Whitney U-test (eosinophils) were applied.¶Results: Control animals showed bi-phasic nasal responses, peaking 10 min and 240 min after the topical antigen challenge, respectively. While the early-phase response was characterized by nasal symptoms of sneezing and scratching accompanied by the increase in TAR, the late-phase was characterized by an increase in TAR accompanied by eosinophil infiltration into nasal mucosa. The nasal symptoms (sneezing and scratching) were not inhibited by pretreatment with ONO-1078 at doses up to 100 mg/kg (p.o., n = 15). Although early peak responses of TAR were not affected with even the highest dose (30 mg/kg, p.o., n = 6), late-phase TAR peak response (control: 174.8 ± 8.2%, n = 6) were significantly inhibited by 10 mg/kg (142.7 ± 15.8%; p 〈 0.05, n = 6) and 30 mg/kg (118.0 ± 6.6%; p 〈 0.01, n = 6) of ONO-1078 (p.o.). In addition, the eosinophil infiltration induced by the antigen was not inhibited by ONO-1078 (30 and 100 mg/kg, p.o., n = 6).¶Conclusions: Our results suggest that Cys LT may play an important role in the late-phase increase in TAR in the guinea pig model of allergic rhinitis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000110050538
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  • 2
    Electronic Resource
    Electronic Resource
    The effects of NK1 receptor antagonists (FK224 and FK888) on agonist- and antigen-induced nasal microvascular leakage in guinea pigs (1997)
    Springer
    Inflammation research 46 (1997), S. 28-31 
    Details
    ISSN: 1420-908X
    Keywords: Key words: Guinea pig — NK1 receptor antagonist — Substance P — Plasma exudation — Nasal allergy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract.   Objective: To study the inhibitory effects of two NK1 receptor antagonists on substance P (SP) and antigen-induced increase of nasal vascular permeability in ovalbumen (OA)-sensitized guinea pigs. ¶Material: Male Dunkin-Hartley guinea pigs. ¶Treatment: SP (100 〈mu〉;mol/l), FK224 (1–10 〈mu〉 mol/kg) and FK888 (0.2– 2 〈mu〉mol/kg). ¶Methods: The in vivo model of nasal microvascular leakage was used for nasal allergic challenge in ovalbumin (OA)-sensitized guinea pigs, or nasal stimulation with substance P (SP) in non-sensitized animals. Nasal microvascular leakage was measured by the accumulation of Evans Blue dye after intravenous injection. ¶Results: Following nasal stimulation with SP 100 〈mu〉M, the concentration of dye in the nasal lavage fluid rapidly increased. NK1 receptor antagonists FK224 (10 〈mu〉mol/kg i.v.) and FK888 (2 〈mu〉mol/kg i.v.) inhibited SP-induced microvascular leakage. In OA-sensitized guinea pigs, exudation of dye into nasal lavage fluid was observed soon after topical antigenic stimulation and continued for over 60 min. Both NK1 receptor antagonists inhibited the immediate phase of the antigen-induced microvascular leakage. ¶Conclusions: We conclude that the immediate change of vascular permeability during the nasal allergic response is mediated by activation of the NK1 receptor in the guinea-pig.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000110050037
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  • 3
    Electronic Resource
    Electronic Resource
    Effects of cyclosporin A and glucocorticosteroids on antigen-induced hypersensitivity to histamine in a guinea pig model of allergic rhinitis (1998)
    Springer
    Inflammation research 47 (1998), S. 62-66 
    Details
    ISSN: 1420-908X
    Keywords: Key words: Hypersensitivity — Allergic rhinitis — Guinea pig — Cyclosporin A — Glucocorticosteroid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Objective and Design: In an attempt to study the pathogenesis of mucosal hypersensitivity in allergic rhinitis, we investigated the suppressive effects of cyclosporin A (CyA) and glucocorticosteroids on ovalbumin (OA)-induced hypersensitivity to topical histamine challenge.¶Materials: Actively sensitized Dunkin-Hartley guinea pigs.¶Treatment: OA and alum were applied to guinea pigs intraperitoneally 3 times at two-week intervals. After general sensitization, OA inhalation was performed every day for 6 days as topical sensitization. Before inhalation, treatment with CyA (50 mg/kg, p.o.), glucocorticosteroids (beclomethasone propionate (1.0 mg/kg, i.p.), fluticasone propionate (FP, 0.5 mg/kg, i.p.)) or vehicle were performed, and the sensitivity to histamine was measured before and after the inhalation. Moreover, in actively (general and topical) sensitized guinea pigs, FP (0.5 mg/kg, i.p.) was applied every day for 5 days and histamine sensitivity was evaluated before and after the application.¶Results: We found that histamine sensitivity was significantly increased by nasal antigen challenge in this guinea pig model, and that the occurrence of histamine hypersensitivity was inhibited by the pretreatment with CyA and glucocorticosteroids. Although multiple administration of FP gradually reduced the histamine hypersensitivity according to the period of administration, it did not significantly alter the histamine hypersensitivity after the occurrence of hypersensitivity.¶Conclusion: It is concluded that CyA and glucocorticosteroids suppress antigen-induced histamine hypersensitivity in a guinea pig model of allergic rhinitis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000110050274
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  • 4
    Electronic Resource
    Electronic Resource
    Effect of glucocorticosteroids on tumour necrosis factor-α-induced intercellular adhesion molecule-1 expression in cultured primary human nasal epithelial cells (2004)
    Oxford, UK : Blackwell Science Ltd
    Clinical & experimental allergy 34 (2004), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Objective In order to confirm the direct effect of glucocorticosteroids on epithelial intercellular adhesion molecule-1 (ICAM-1) expression, we examined ICAM-1 expression on primary cultured human nasal epithelial cells (HNECs) at both protein and mRNA levels.Material and methods HNECs were stimulated with recombinant human TNF-α (20 pg/mL–20 ng/mL) for specified time periods (0, 12, 24, and 48 h) and ICAM-1 mRNA and the soluble ICAM-1 (sICAM-1) concentrations were measured by quantitative RT-PCR and ELISA, respectively. We also evaluated surface expression of ICAM-1 by flow cytometry 48 h after stimulation and determined the effect of dexamethasone (DEX) on TNF-α-induced ICAM-1 expression.Results Significant increases in ICAM-1 gene expression in HNECs were initially detected at 24 h, peaking at 48 h after the stimulation. The TNF-mediated-ICAM-1 mRNA and ICAM-1 surface expression at 48 h was significantly inhibited by co-incubation with human recombinant soluble TNF receptor I. Similarly, TNF-α-induced release sICAM-1 occurred in a time- and concentration-dependent manner. DEX 10−6 m attenuated the TNF-α-induced ICAM-1 expression at mRNA and protein levels.Conclusions Our finding suggests a potential role for topical steroids in allergic rhinitis in suppressing inflammatory reactions in the nasal mucosa by regulating ICAM-1 expression on nasal epithelium.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.2004.01964.x
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  • 5
    Electronic Resource
    Electronic Resource
    Expression and localization of the cysteinyl leukotriene 1 receptor in human nasal mucosa (2002)
    Oxford, UK : Blackwell Science Ltd
    Clinical & experimental allergy 32 (2002), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background The cysteinyl leukotrienes (CysLT) are lipid mediators that have been implicated in the pathogenesis of allergic diseases. Pharmacological studies using CysLTs indicate that two classes of receptors, named CysLT1 and CysLT2 receptor, exist. The former is sensitive to the CysLT1 antagonist currently used to treat asthma and allergic rhinitis. Recently, the cDNA for human CysLT1 and CysLT2 receptor have been cloned, making it now possible to study the gene expression of CysLTs receptors.Objective We have used reverse transcription and polymerase chain reaction (RT-PCR) to study the gene expression of CysLT1 and CysLT2 receptor and in situ hybridization to determine the distribution of CysLT1 receptor mRNA in human nasal mucosa. In addition, the distribution of the CysLT1 receptor protein was studied by immunohistochemistry.Methods Human turbinates were obtained after turbinectomy from six patients with nasal obstruction refractory to medical therapy. Total RNA was isolated from human nasal mucosa and both CysLT1 and CysLT2 receptor mRNA was detected in these tissues by using RT-PCR. For in situ hybridization study of human nasal mucosa, we used biotin-labelled oligonucleotides probes encoding human CysLT1 receptor cDNA. To identify the cells expressing the CysLT1 receptor protein, double immunostaining was performed by using anti-CysLT1 receptor antibody and monoclonal antileucocyte antibodies.Results RT-PCR analysis of total nasal RNA demonstrated the expression of both CysLT1 receptor and CysLT2 receptor mRNA. In situ hybridization indicated high levels of CysLT1 receptor hybridization in blood vessels and the interstitial cells, but a sparse signal in airway epithelium and submucosal glands. The immunohistochemical studies revealed that anti-CysLT1 receptor antibody labelled eosinophils, mast cells, macrophages, neutrophils and vascular endothelial cells in the nasal mucosa.Conclusion The results may have an important clinical implication and also promote further investigation of the regulation of CysLT1 receptor in health and disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2222.2002.01425.x
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  • 6
    Electronic Resource
    Electronic Resource
    Establishment of Animal Model of Antigen-Specific T Lymphocyte Recruitment into Nasal Mucosa (2002)
    Oxford, UK : Blackwell Science Ltd
    Scandinavian journal of immunology 56 (2002), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: DO11.10 transgenic mice, expressing an ovalbumin (OVA)-specific αβ T-cell receptor (TCR), have been used as a model of various immune diseases associated with T lymphocytes. Some studies of immunoresponse in lung have involved adoptive transfer of DO11.10 mice. As of yet, however, there have been no studies of the adoptive transfer model in the upper airway. The purpose of this study was to establish an animal model to clarify the recruitment mechanism and the roles of Th2 cells in allergic rhinitis. In accordance with the adoptive transfer system, we generated Th0, Th1 and Th2 cells from DO11.10 mice and transferred them into wild type BALB/c mice. Following nasal OVA challenge to DO11.10 mice or to the BALB/c mice into which antigen-specific Th2 cells had been transferred, the number of local antigen-specific TCR-positive cells accompanying the local eosinophilia had significantly increased. However, nasal OVA challenge to BALB/c mice into which antigen-specific Th0 or Th1 cells were transferred failed to increase the number of local OVA-specific TCR positive cells. These observations suggest that an antigen-specific homing mechanism of Th2 cells may exist in nasal mucosa. Analysis of this model will assist in the development of new therapeutic strategy, which targets Th2 cells in allergic rhinitis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-3083.2002.01136.x
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  • 7
    Electronic Resource
    Electronic Resource
    Photochemical reaction of friedelin with acetone
    Amsterdam : Elsevier
    Tetrahedron Letters 16 (1975), S. 2271-2274 
    Details
    ISSN: 0040-4039
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/S0040-4039(00)75098-2
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  • 8
    Electronic Resource
    Electronic Resource
    Inhibitory effects of azelastine on nasal allergic responses in sensitized guinea pigs (1992)
    Springer
    European archives of oto-rhino-laryngology and head & neck 249 (1992), S. 279-282 
    Details
    ISSN: 1434-4726
    Keywords: Nasal allergy ; Vascular permeability ; Leukotrienes ; Guinea pig ; Azelastine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The in vivo effects of the antiallergic drug azelastine were investigated in sensitized guinea pigs. Topical administration of antigen into the nasal cavity produced an increase in nasal vascular permeability together with an increase in both the histamine and leukotriene C4 (LTC4) concentrations of nasal lavage fluid. Pre-treatment with azelastine significantly inhibited both the LTC4 release and the increase in nasal vascular permeability. These results suggest that azelastine inhibits the release of antigen-induced leukotrienes and increases nasal vascular permeability in vivo.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00714493
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