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Aureus Enterotoxin B (aureu + enterotoxin_b)

Distribution by Scientific Domains
Medical Sciences80%

Kinds of Aureus Enterotoxin B

  • staphylococcus aureu enterotoxin b
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    Selected Abstracts

    Non-enzymatic aqueous peroxyoxalate chemiluminescence immune detection using a CCD camera and a CMOS device

    LUMINESCENCE: THE JOURNAL OF BIOLOGICAL AND CHEMICAL LUMINESCENCE, Issue 5 2008
    Brian Filanoski
    Abstract A new method for non-enzymatic aqueous peroxyoxalate chemiluminescence (POCL) biomolecular detection using imaging chip-based devices has been developed. A water-soluble amide of oxalic acid was synthesized and used in the investigation and characterization of POCL immunodetection in an aqueous environment. Six fluorescent dyes commonly used in biological detection were tested, and the intensity of light generated from the aqueous POCL reactions was characterized in the liquid phase. Direct detection sensitivity comparisons between a standard fluorescent method and this POCL method were performed in both liquid and solid phases. Results showed that detection sensitivity using the POCL method is comparable to that of the fluorescent method. POCL biomolecular detection on a nitrocellulose membrane was also investigated using a charge-coupled device (CCD) camera. Again, POCL detection sensitivity proved to be comparable to that using the fluorescent detection method. In an application of aqueous POCL biomolecular detection, Staphylococcus aureus enterotoxin B (SEB) and its antibody were used to demonstrate immuno- and affinity detection. For further applications, such as DNA and protein arrays, simultaneous detection of biomolecules labelled with different fluorescent labels was investigated, using a complementary metal oxide semiconductor (CMOS) colour imaging chip. Copyright © 2008 John Wiley & Sons, Ltd. [source]

    Staphylococcus aureus enterotoxin B augments granulocyte migration and survival via airway epithelial cell activation

    ALLERGY, Issue 8 2010
    W. Huvenne
    To cite this article: Huvenne W, Callebaut I, Reekmans K, Hens G, Bobic S, Jorissen M, Bullens DMA, Ceuppens JL, Bachert C, Hellings PW. Staphylococcus aureus enterotoxin B augments granulocyte migration and survival via airway epithelial cell activation. Allergy 2010; 65: 1013,1020. Abstract Background:,Staphylococcus aureus enterotoxin B (SEB) has recently been postulated to be involved in the pathology of granulocyte-dominated disease. Studying the immunologic interaction between SEB and airway epithelial cells in immortalized cell lines or long-term epithelial cell cultures has obvious disadvantages. Methods:, We used a novel technique of freshly isolated and purified human nasal epithelial cells (HNEC) from healthy, nonallergic individuals, which were incubated for 24 h without/with SEB at different concentrations. Chemokine production was evaluated in the supernatant using Cytometric Bead Array. The chemotactic activity of the supernatant was studied in vitro using a Boyden chamber. Survival was evaluated with flow cytometry, using propidium iodide to identify dead cells. Results:,Staphylococcus aureus enterotoxin B showed a dose-dependent induction of interferon-inducible protein-10, monokine induced by interferon-,, regulated upon activation normal T cell expressed and secreted, monocyte chemoattractant protein 1 (MCP-1) and granulocyte colony stimulating factor production by epithelial cells in vitro. The supernatant of epithelial cells had chemotactic activity for granulocytes in vitro, which was enhanced in the supernatant of SEB-stimulated epithelial cells. Reduced number of propidium iodide positive granulocytes was found in the conditions where supernatant of SEB-stimulated epithelial cells was applied. Conclusion:,Staphylococcus aureus enterotoxin B exerts a direct pro-inflammatory effect on HNEC, with induction of chemokine and growth factor release, resulting in the migration and prolonged survival of granulocytes in vitro. [source]

    T cell inflammatory response, Foxp3 and TNFRS18-L regulation of peripheral blood mononuclear cells from patients with nasal polyps-asthma after staphylococcal superantigen stimulation

    CLINICAL & EXPERIMENTAL ALLERGY, Issue 9 2010
    C. A. Pérez Novo
    Cite this as: C. A. Pérez Novo, M. Jedrzejczak-Czechowicz, A. Lewandowska-Polak, C. Claeys, G. Holtappels, P. Van Cauwenberge, M. L. Kowalski and C. Bachert, Clinical & Experimental Allergy, 2010 (40) 1323,1332. Summary Background Staphylococcal superantigens may modulate airway inflammatory disease. Objective We assessed the effect of Staphylococcus aureus enterotoxin B (SEB) on T cell activation in patients with nasal polyps and asthma, and its possible link to aspirin hypersensitivity. Methods Leucocytes were isolated from five healthy subjects (controls), five asthmatics with nasal polyps without (NP-ATA) and five with aspirin-induced asthma (NP-AIA). Cells were incubated with increasing concentrations of SEB for 4 and 18 h. Release of TH1/TH2 cytokines was assessed by Cytometric Bead-Array. Foxp3 and TNFRS18-L expression were analysed by qPCR and flow cytometry. Results After 4 and 18 h, SEB significantly increased IFN-gamma, IL-4, TNF-alpha, IL-5 and IL-2 concentrations in supernatants of both NP polyp groups compared with controls. Baseline Foxp3 was significantly decreased in both NP-asthma groups. Incubation with SEB for 4 h induced a limited up-regulation of Foxp3 in NP-AIA patients, which was switched off consecutively. Foxp3 was significantly up-regulated in the control group after 18 h, but not in the NP-asthmatic groups. In parallel, TNFRS18-L mRNA significantly increased after 18 h in the NP-asthma groups compared with control subjects. This molecule was highly expressed in CD11c+CD14+ cells and its levels increased after 18 and 24 h culture in the NP-asthma patients. Conclusion SEB induces both TH1 and TH2 pro-inflammatory responses in patients with nasal polyps and asthma regardless of the presence of aspirin hypersensitivity. The nature of this response may be linked to a basal deficiency of Foxp3 observed in the NP-asthmatic patients and/or to the up-regulation of TNFRS18-L on monocytes/dendritic cell precursors. [source]

    Aggravation of bronchial eosinophilia in mice by nasal and bronchial exposure to Staphylococcus aureus enterotoxin B

    CLINICAL & EXPERIMENTAL ALLERGY, Issue 8 2006
    P. W. Hellings
    Summary Background The role of bacterial enterotoxins like Staphylococcus aureus enterotoxin B (SEB) in allergic asthma remains unknown. We used a mouse model of airway allergy to study the effects of nasal or bronchial contact with SEB on bronchial allergic inflammation. Methods The features of allergic asthma were induced in ovalbumin (OVA)-sensitized mice (days 1,13) by repeated exposures to nebulized OVA (days 33,37). Nasal or bronchial application of SEB was performed on three occasions (days 33,35,37), and the effects on bronchial inflammation, IgE titres and expression levels of mRNA for T helper type 2 cytokines and other inflammatory mediators were evaluated. Results Both nasal and bronchial SEB enhanced the allergen-induced bronchial inflammation, as reflected by more eosinophilic inflammation in the airway lumen and in bronchial tissue. Aggravation of experimental asthma correlated with higher expression of mRNA for IL-5, IL-4, IFN-,, IL-12 p40, eotaxin-1 and TGF-, in bronchi. In addition, nasal SEB elevated concentrations of IL-4, IL-5 and IFN-, in serum and bronchial SEB increased titres of OVA-specific and total IgE in serum. Conclusion Our data illustrate the potential of both nasal as well as bronchial SEB to aggravate several features of allergic asthma in a mouse model. [source]