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  • 1
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Pharmacology 25 (1985), S. 381-412 
    ISSN: 0362-1642
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Regulated on activation, normal T cells expressed and secreted (RANTES) is a member of the CC chemokine family and contributes to viral-induced airway inflammation including exacerbations of asthma. Double-stranded RNA (dsRNA) is known to be synthesized during replication of many viruses and a ligand of Toll-like receptor 3. We hypothesized that dsRNA may mimic viral infection and induce RANTES expression in airway epithelial cells.Objective We first confirmed that dsRNA up-regulated RANTES mRNA and protein synthesis in the airway epithelial cells. We next focused our studies on the transcriptional regulation of RANTES.Methods Airway epithelial cell line BEAS-2B and normal human bronchial epithelial cells were used in vitro study. Levels of RANTES mRNA and protein expression were determined with RT-PCR and ELISA. Mechanisms of transcriptional regulation were assessed by electrophoretic mobility shift assay and dual luciferase assay using RANTES promoter-luciferase reporter plasmids.Results Activation of nuclear factor-κB (NF-κB) was confirmed by nuclear protein binding to a DNA probe derived from the RANTES promoter. Activity of the RANTES promoter was increased by dsRNA. The stimulation with dsRNA was partially inhibited in plasmids mutated at either of the binding sites for NF-κB or IFN regulatory factors (IRFs). When both sites were mutated, the activation was totally abrogated.Conclusion These results imply that dsRNA activates NF-κB and IRFs and these transcription factors activate transcription of the RANTES promoter and its protein expression in airway epithelial cells.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Activation of signal transducer and activator of transcription (STAT)6 by IL-4 and IL-13 is essential in many key epithelial responses in the asthmatic airway including expression of numerous chemokines, goblet cell differentiation and mucus production and expression of other allergic inflammatory genes. While these responses are all inhibited by glucocorticoids (GC) administered systemically or by inhalation, the inhibitory mechanisms are unknown.Objective To test the hypothesis that GC suppress allergic responses by blocking IL-4-induced STAT6 signalling in airway epithelial cells.Methods Western blotting and reporter gene assays were used to determine whether GC could inhibit STAT6 production, phosphorylation or nuclear translocation, or whether GC could affect STAT6 transcriptional activity in the BEAS-2B airway epithelial cell line.Results Our results showed that GC had no inhibitory effect on the total cellular or nuclear levels of STAT6 or phospho-STAT6. GC did not inhibit transcription from three different STAT6-driven reporter constructs, indicating that GC also did not inhibit STAT6 function.Conclusion We conclude that airway epithelial STAT6 is not the central target of GC in allergic inflammation and that the inhibitory effect of GC on STAT6-mediated IL-4- and IL-13-induced responses is exerted by targeting pathways distinct from STAT6.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Clinical & experimental allergy 31 (2001), S. 0 
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Desloratadine is a non-sedating, clinically effective, anti-allergic therapy that has been shown to exhibit anti-inflammatory properties that extend beyond its ability to antagonize histamine at H1-receptor sites. This latter effect has been shown in vitro to be both IgE-dependent and -independent.Objective In this study, we addressed the ability of desloratadine to inhibit the in vitro generation of interleukin (IL)-4 and IL-13 from human basophils while concurrently comparing its efficacy in preventing mediator release by these cells.Methods Basophil-enriched suspensions were treated with various concentrations of desloratadine for 15 min before stimulating with either anti-IgE antibody, calcium ionophore, IL-3 or phorbol ester. Histamine (fluorimetry), LTC4 (RIA) and IL-4 (ELISA) were all assayed using the same 4-h culture supernatants. IL-13 (ELISA) was measured in supernatants harvested after 20 h incubation. IL-4 mRNA expression (dilutional RT-PCR) was also examined.Results Desloratadine was found to be nearly six–seven times more potent in preventing the secretion of IL-4 and IL-13 induced by anti-IgE than it was at inhibiting the release of histamine and LTC4. These cytokines were equally inhibited by desloratadine following activation with ionomycin despite the lack of an effect on the histamine induced with ionomycin. Desloratadine had a lesser effect regarding inhibition of the IL-13 secreted in response to IL-3 and PMA. There was no evidence that desloratadine mediated its inhibitory effects by causing decreased cell viability. Finally, IL-4 mRNA accumulation was remarkably inhibited, by as much as 80%, following pretreatment with desloratadine.Conclusion While capable of inhibiting histamine and LTC4 release by human basophils, desloratadine is more effective at targeting the signals regulating IL-4 and IL-13 generation in these cells. This inhibitory effect on cytokine generation provides additional evidence that this antihistamine exerts anti-inflammatory properties.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    European journal of clinical pharmacology 45 (1993), S. S3 
    ISSN: 1432-1041
    Keywords: Glucocorticoid ; Anti-inflammatory ; allergy ; cytokine ; osinophil ; neutrophil ; leucocyte
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Glucocorticoids (GC) exert a variety of important anti-inflammatory actions. We have studied their effects in allergic inflammation and believe that their antiallergic effects reflect their anti-inflammatory activities in general. These effects include inhibition of cytokine and other mediator secretion, inhibition of leucocyte priming in eosinophils and neutrophils, reduction of vascular permeability, inhibition of arachidonic acid metabolite and platelet activating factor (PAF) release, synergistic or permissive effects on responses to other mediators, such as catecholamines and other endogenous hormone-like molecules, and modulation of enzyme systems involved in inflammation. Glucocorticoid actions are thus multifaceted; this feature explains both their unequalled efficacy in inflammatory diseases and the difficulty in replacing them with other medications that have a uni-dimensional profile of action.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    European journal of clinical pharmacology 45 (1993), S. S43 
    ISSN: 1432-1041
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-1750
    Keywords: Granulocyte/macrophage colony-stimulating factor ; Glucocorticoids ; Lung
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Granulocyte/macrophage colony-stimulating factor (GM-CSF) is an important hematopoietic growth factor which has been shown to induce proliferation and activation of inflammatory cells, and may play a role in allergic diseases and experimental allergic reactions. Since little is known about the involvement of cytokines in allergic inflammation in the lung, we investigated whether human lung fragments produce GM-CSF in vitro. The present studies demonstrate that human lung fragments produce GM-CSF in vitro and that glucocorticoids are potent inhibitors of this cytokine production. Human lung was cut into fragments, rinsed, and cultured in 60-mm tissue culture plates containing 50 mg of tissue in RPMI 1640 with antibiotics in the presence or absence of a variety of steroids for 18 h. Lung fragments were rinsed and then incubated for an additional 4 h. Supernatants were harvested and analyzed for GM-CSF activity using the GM-CSF/interleukin (IL)-3 responsive M-07e human luekemic cell line. Steroids alone had no effect on M-07e proliferation. Human lung fragments produced 32.1 ± 11.8 ng of GM-CSF equivalents per gram wet weight of tissue during the 4 h incubation (mean ± S.E.M., n = 5, range 9.2–74.2). While specific antisera against human GM-CSF neutralized 96.8 ± 2.8% (n = 5) of the activity, anti-IL-3 antibody had no effect, suggesting most or all of this activity was GM-CSF. Treatment of lung fragments in vitro for 18 h with hydrocortisone (HC) inhibited the production of GM-CSF dose-dependently. Maximal inhibition of GM-CSF production was 72.8 ± 4.0% at a concentration of 10−6 m hydrocortisone (n = 5), and the molar concentration of HC that inhibited of GM-CSF production by lung tissue by 50% (IC50) was approximately 4.5 × 10−7 m. Kinetic studies revealed that a 6 h preincubation with the drug was required for 50% inhibition of GM-CSF production. HC and other glucocorticoids, at a concentration of 0.1 µm, demonstrated significant inhibition of GM-CSF release. Based on the rank order of potency of several glucocorticoids, and the fact that nonglucocorticoid steroids including testosterone and β-estradiol (0.1 µm) had no effect, we suggest that this is a specific receptor-mediated effect. We conclude that human lung produces GM-CSF in vitro and that antiinflammatory steroids are potent and effective inhibitors of the production of this cytokine. This may contribute to the therapeutic efficacy of these drugs in pulmonary diseases.
    Type of Medium: Electronic Resource
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  • 8
    Publication Date: 2013-03-01
    Description: Key Points Mature, but not immature, dendritic cells are sensitive to glucocorticoid-induced apoptosis. Mature, but not immature, dendritic cells express proapoptotic glucocorticoid receptor translational isoforms.
    Keywords: Immunobiology
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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  • 9
    Publication Date: 2015-08-08
    Description: Mast cells are critical in the pathogenesis of allergic disease due to the release of preformed and newly synthesized mediators, yet the mechanisms controlling mast cell activation are not well understood. Members of the tetraspanin family are recently emerging as modulators of FcRI-mediated mast cell activation; however, mechanistic understanding of their function is currently lacking. The tetraspanin CD151 is a poorly understood member of this family and is specifically induced on mouse and human mast cells upon FcRI aggregation but its functional effects are unknown. In this study, we show that CD151 deficiency significantly exacerbates the IgE-mediated late phase inflammation in a murine model of passive cutaneous anaphylaxis. Ex vivo, FcRI stimulation of bone marrow–derived mast cells from CD151 –/– mice resulted in significantly enhanced expression of proinflammatory cytokines IL-4, IL-13, and TNF-α compared with wild-type controls. However, FcRI-induced mast cell degranulation was unaffected. At the molecular signaling level, CD151 selectively regulated IgE-induced activation of ERK1/2 and PI3K, associated with cytokine production, but had no effect on the phospholipase C1 signaling, associated with degranulation. Collectively, our data indicate that CD151 exerts negative regulation over IgE-induced late phase responses and cytokine production in mast cells.
    Print ISSN: 0022-1767
    Electronic ISSN: 1550-6606
    Topics: Medicine
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  • 10
    Publication Date: 2015-08-22
    Description: The G-protein–coupled protease-activated receptor 2 (PAR2) plays an important role in the pathogenesis of various inflammatory and auto-immune disorders. In airway epithelial cells (AECs), stimulation of PAR2 by allergens and proteases triggers the release of a host of inflammatory mediators to regulate bronchomotor tone and immune cell recruitment. Activation of PAR2 turns on several cell signaling pathways of which the mobilization of cytosolic Ca 2+ is likely a critical but poorly understood event. In this study, we show that Ca 2+ release-activated Ca 2+ (CRAC) channels encoded by stromal interaction molecule 1 and Orai1 are a major route of Ca 2+ entry in primary human AECs and drive the Ca 2+ elevations seen in response to PAR2 activation. Activation of CRAC channels induces the production of several key inflammatory mediators from AECs including thymic stromal lymphopoietin, IL-6, and PGE 2 , in part through stimulation of gene expression via nuclear factor of activated T cells (NFAT). Furthermore, PAR2 stimulation induces the production of many key inflammatory mediators including PGE 2 , IL-6, IL-8, and GM-CSF in a CRAC channel–dependent manner. These findings indicate that CRAC channels are the primary mechanism for Ca 2+ influx in AECs and a vital checkpoint for the induction of PAR2-induced proinflammatory cytokines.
    Print ISSN: 0022-1767
    Electronic ISSN: 1550-6606
    Topics: Medicine
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