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  • 1
    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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  • 2
    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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  • 3
    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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