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  • Digitale Medien  (6)
  • 1995-1999  (6)
  • 1
    Digitale Medien
    Digitale Medien
    Bronchial hyperresponsiveness and airway neutrophil accumulation induced by interleukin-8 and the effect of the thromboxane A2 antagonist S-1452 in guinea-pigs (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 25 (1995), S. 0 
    Details
    ISSN: 1365-2222
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Interleukin-8 (IL-8) has been shown to be a chemotactic factor for neutrophils, T-lymphocytes and eosinophils, but it is unknown whether the IL-8-induced inflammatory cell accumulation into the airways can cause the bronchial hyperresponsiveness (BHR) characteristic of asthma. IL-8 at a dose of 0.5 or 5μg/kg was administered intranasally to guinea-pigs twice a week for 3 weeks. One day after the last administration, animals were anesthetized and artificially ventilated through tracheal cannula and lateral pressure at the cannula (Pao) was measured as an overall index of airway responses to increasing concentrations of inhaled histamine (25, 50, 100, and 200 μg/ml). The IL-8 treatment significantly enhanced bronchial responsiveness to histamine in a dose-dependent manner (ANOVA P 〈 0.01). The provocative concentration of histamine causing a 100% increase in Pao (PC100) at a dose of 0.5 and 5μg/kg of IL-8 was 68.1 (Gsem 1.12) and 35.6 (Gsem 1.25) μg/ml, respectively. The latter was significantly (P 〈 0.01) lower than that in control animals treated with PBS (93.3 [Gsem, 1.14] μg/ml)- The IL-8 treatment also induced a significant influx of neutrophils, but not eosinophils, in bronchoalveolar lavage (BAL) fluid (18.3 ± 8.8 and 30.6 ± 8.3% in animals treated with 0.5 and 5 μg/kg, respectively, of IL-8 vs 3.6 ± 0.7% in phosphate buffered saline-(PBS)-treated animals). Furthermore, we examined the effect of the thromboxane receptor antagonist S-1452 (0.01 or 0.1 mg/kg, i.p. 24 and 1 h before anesthesia) on this IL-8 induced BHR. S-1452 significantly inhibited the BHR dose-dependently (ANOVA P 〈 0.001). PC100 was 94.0 (Gsem 1.19), 137.4 (Gsem 1.17) and 43.0 (Gsem 1.24) μg/ml with S-1452 at doses of 0.01 and 0.1mg/ml and saline, respectively. We conclude that IL-8 causes BHR and airway neutrophil inflammation, and that thromboxane A2 is important in the development of BHR induced by IL-8.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1111/j.1365-2222.1995.tb01002.x
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  • 2
    Digitale Medien
    Digitale Medien
    Sensory neuropeptides are not directly involved in bronchial hyperresponsiveness induced by interleukin-8 in guinea-pigs in vivo (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 26 (1996), S. 0 
    Details
    ISSN: 1365-2222
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Background Interleukin-8 (IL-8) hus been shown to be a chemotactic factor for netitrophils, T-lymphocytes and eosinophils. Repeated intranasal administration of IL-8 enhances bronchial responsiveness to inhaled histamine in guinea-pigs. Neuropeptides which arc released trotn C-fibre nerve-endings have been postulated to induce bronchial hyperresponsiveness through neurogenic inflammation.Objective This study was conducted to examine whether sensory neuropeptides are involved in the IL-8-induced bronchial hyperresponsiveness.Methods IL-8 at a dose of 5μg/kg was administered intranasally to guinea-pigs twice a week for 3 weeks. One day after the last administration, animals were anesthetized and artificially ventilaled through tracheal cannula, and lateral pressure at the tracheal cannula (Pao) was measured as an overall index of airway responses lo increasing concentrations of inhaled histamine (25, 50, 100, and 200 μg/mL). A NKI and NK2 dual antagonist FK224(10mg/kg), a selective NK1 antgonist FK888 (10mg/kg) or vehicle was intravenously administered 10min before measurement of bronchial responsiveness.Result The IL-8 treatment significantly enhanced bronchial responsiveness to histamine (ANOVA P 〈 0.01). FK224 or FK888 did not alter the IL-8-induced bronchial hyperresponsiveness.Conclusion We conclude that repeated intranasal administratioti of IL-8 causes bronchial hyperresponsiveness (BHR) and that neuropeptides such as neurokinin A and substance P do not directly contribute to the development of BHR induced by IL-8.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1111/j.1365-2222.1996.tb00103.x
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  • 3
    Digitale Medien
    Digitale Medien
    Eosinophilopoietic factors prime eosinophils for increased interleukin-8 generation (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Allergy 52 (1997), S. 0 
    Details
    ISSN: 1398-9995
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Recent studies have identified eosinophils as a cellular source of various cytokines, indicating that eosinophils play not only an effector role but also a regulatory role within the allergic inflammatory cell network. Because eosinophilopoietic factors are known to stimulate various functions of eosinophils, we examined the effect of interleukin (IL)-5 on chemoattractant-induced IL-8 generation from eosinophils. Although IL-5 alone induced little or no IL-8 production from eosinophils, short-term preincubation with IL-5 markedly enhanced the eosinophil IL-8 generation caused by C5a plus cytochalasin B (CB). IL-3 also potentiated C5a-induced IL-8 generation. Both factors were active at picomolar concentrations. Furthermore, competitive polymerase chain reaction (PCR) experiments revealed that the enhancement occurred at the pretranslational level. Since eosinophils in allergic inflammation are believed to be activated by these eosinophilopoietic factors, eosinophil-derived cytokines may play more important roles in the allergic inflammatory cell network than has been previously supposed.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1111/j.1398-9995.1997.tb00997.x
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  • 4
    Digitale Medien
    Digitale Medien
    Interleukin-8 inhalation directly provokes bronchoconstriction in guinea pigs (1999)
    Copenhagen : Munksgaard International Publishers
    Allergy 54 (1999), S. 0 
    Details
    ISSN: 1398-9995
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Background: Although it has been reported that the concentration of interleukin (IL)-8 in nasal lavage fluid and sputum and its production in bronchial epithelium were increased in asthmatic subjects, the direct effects of IL-8 on the airways in vivo is unclear. Methods: We examined bronchoconstriction in response to IL-8 inhalation through an endotracheal cannula in anesthetized, artifically ventilated guinea pigs. Results: Inhalation of IL-8 at concentrations of 1 and 10 μg/ml caused significant bronchoconstriction, as revealed by the elevation of pressure at the airway opening. Moreover, the bronchoconstriction induced by IL-8 was significantly inhibited by the antihistamines diphenhydramine and terfenadine, suggesting the involvement of histamine release in the IL-8-induced bronchoconstriction. No significant leukocyte infiltration was observed in the bronchoalveolar lavage fluid or histologic findings 25 min after the first IL-8 inhalation. Conclusions: IL-8 provokes bronchoconstriction without leukocyte accumulation in the airways, mediated in part by histamine release, in guinea pigs.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1034/j.1398-9995.1999.00891.x
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  • 5
    Digitale Medien
    Digitale Medien
    Inhibition of neutrophil-mediated acute inflammatory injury by an antibody against interleukin-8 (IL-8) (1998)
    Springer
    Inflammation research 47 (1998), S. 151-157 
    Details
    ISSN: 1420-908X
    Schlagwort(e): Key words: Interleukin-8 — Neutrophil — Acute inflammation — Cerebral reperfusion injury — Acute respiratory distress syndrome
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract. Chemokines are a family of cytokines regulating the migration and functions of leukocytes in a cell-type specific manner. A prototype of C-X-C chemokines, interleukin-8 (IL-8), chemoattracts and activates neutrophils in vitro, and IL-8 concentrations in body fluids are markedly increased in several neutrophil-mediated acute inflammation. Moreover, we previously reported that the administration of a neutralizing antibody to IL-8 prevented neutrophil-mediated tissue injury, as well as neutrophil infiltration, in several animal disease models. These observations implicate IL-8 as a major mediator of neutrophil-mediated tissue injury. Furthermore, we recently showed that an anti-IL-8 antibody effectively prevented two models that are very relevant to clinical situations; endotoxemia-induced acute respiratory distress syndrome (ARDS)-like lung injury and cerebral reperfusion injury. These results raise the possibility that IL-8 is a novel target for therapeutic intervention in neutrophil-mediated acute inflammation.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/s000110050308
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  • 6
    Digitale Medien
    Digitale Medien
    Dissociation of ligand-induced internalization of CXCR-4 from its co-receptor activity for HIV-1 Env-mediated membrane fusion (1998)
    Springer
    Archives of virology 143 (1998), S. 851-861 
    Details
    ISSN: 1432-8798
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary.  The C-terminal cytoplasmic tail of chemokine receptors is important for their internalization upon ligand binding. We generated several deletion mutants of the C-terminal cytoplasmic tail of CXCR-4, a co-receptor for T cell line tropic strains of human immunodeficiency virus type 1 (HIV-1), to know whether or not co-receptor internalization is associated with HIV-1 entry. Our data showed that the removal of C-terminal 15 amino acid residues of the cytoplasmic tail from CXCR-4 completely abolished its internalization, but did not affect the co-receptor activity at all. Co-receptor activity was fully retained even when all 45 amino acid residues in the C-terminal cytoplasmic tail had been deleted. These data indicated that no cytoplasmic tail nor internalization of CXCR-4 is required for its co-receptor activity for HIV-1 entry.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/s007050050337
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