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  • 1
    Electronic Resource
    Electronic Resource
    Alpha-toxin is produced by skin colonizing Staphylococcus aureus and induces a T helper type 1 response in atopic dermatitis (2005)
    Oxford, UK : Blackwell Science Ltd
    Clinical & experimental allergy 35 (2005), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Staphylococcus aureus is a well known trigger factor of atopic dermatitis (AD). Besides the superantigens, further exotoxins are produced by S. aureus and may have an influence on the eczema.Objective To explore the impact of staphylococcal α-toxin on human T cells, as those represent the majority of skin infiltrating cells in AD.Methods Adult patients with AD were screened for cutaneous colonization with α-toxin producing S. aureus. As α-toxin may induce necrosis, CD4+ T cells were incubated with sublytic α-toxin concentrations. Proliferation and up-regulation of IFN-γ on the mRNA and the protein level were assessed. The induction of t-bet translocation in CD4+ T cells was detected with the Electrophoretic Mobility Shift Assay.Results Thirty-four percent of the patients were colonized with α-toxin producing S. aureus and α-toxin was detected in lesional skin of these patients by immunohistochemistry. Sublytic α-toxin concentrations induced a marked proliferation of isolated CD4+ T cells. Microarray analysis indicated that α-toxin induced particularly high amounts of IFN-γ transcripts. Up-regulation of IFN-γ was confirmed both on the mRNA and the protein level. Stimulation of CD4+ T cells with α-toxin resulted in DNA binding of t-bet, known as a key transcription factor involved into primary T helper type 1 (Th1) commitment.Conclusion α-toxin is produced by S. aureus isolated from patients with AD. We show here for the first time that sublytic α-toxin concentrations activate T cells in the absence of antigen-presenting cells. Our results indicate that α-toxin is relevant for the induction of a Th1 like cytokine response. In AD, this facilitates the development of Th1 cell dominated chronic eczema.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.2005.02295.x
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  • 2
    Electronic Resource
    Electronic Resource
    Deficiency in immunoglobulin G2 antibodies against staphylococcal enterotoxin C1 defines a subgroup of patients with atopic dermatitis (2005)
    Oxford, UK : Blackwell Science Ltd
    Clinical & experimental allergy 35 (2005), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background and aim Atopic dermatitis (AD) is a common chronic inflammatory skin disease often accompanied by cutaneous Staphylococcus aureus colonization and, in this regard, especially complicated by the presence of superantigen-producing strains. Because IgG antibodies comprise an important defence mechanism of the adaptive immune system against bacteria, it was investigated whether AD patients have an abnormal pattern or distribution of superantigen-specific IgG subclass antibodies in association with disease severity and activity.Methods Staphylococcal enterotoxin B (SEB) and staphylococcal enterotoxin C1 (SEC1) specific IgG antibody subclasses were assessed in n=89 adult AD patients with mild to severe disease activity as determined by the SCORAD score and in n=28 healthy age-matched controls. Results were correlated with the current status of bacterial skin colonization and severity score.Results Thirty-eight per cent of the AD patients showed a selective deficiency in IgG2 antibodies against SEC1 compared with only 14% in the control group. The absence of these antibodies was found in both currently colonized and non-colonized AD patients and was associated with a severe phenotype (SCORAD more than 40 points in two-thirds of the deficient patients). However, these patients had normal production levels of IgG2 antibodies against pneumococcal capsular polysaccharide (PCP) and SEB, but higher IgG1 and IgG4 titres against SEC1. Except for elevated total IgG1, total IgG subclass levels were normal in this AD subgroup. Yet, peripheral blood mononuclear cells (PBMCs) derived from these patients clearly produced IL-4 and IL-5 upon SEC1 re-stimulation whereas PBMCs from those providing SEC1-specific IgG2 antibodies failed in the production of these cytokines.Conclusion A subgroup of AD patients suffers from a selective deficiency to produce anti-SEC1 IgG2 antibodies. This patient group is characterized by a severe AD phenotype.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.2005.02192.x
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    Paper (German National Licenses)
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