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K Neuber

Publications and source records attributed to K Neuber.

30 records · Page 2Linked to original sources
PubMed1993

[Staphylococcus aureus and atopic eczema].

The bacterial skin flora of patients with atopic eczema is different from that in healthy normal persons. In addition, such patients more often suffer from microbial infections. Differences in sebum and sweat secretion and increased bacterial adhesion to epithelial cells in atopic eczema may predispose to enhanced amounts of Staphylococcus aureus, for example, on the skin. Defective host-defence mechanisms with dysfunction of cellular and humoral immune reactions have been suggested. On the other hand, bacterial antigens may induce allergic reactions, e.g. increased IgE synthesis and enhanced expression of the low-affinity receptor for IgE (CD23, Fc epsilon RII), and the release of inflammatory mediators such as leukotrienes and histamine. The production of bacterial toxins might be important for the pathophysiology of atopic eczema. This paper summarizes the present data and tries to integrate them into a model for the induction of atopic eczema.

B-Lymphocytes↗
PubMed1992

Atopic eczema: role of microorganisms on the skin surface.

The pathophysiology of atopic eczema (AE) is still poorly understood. One possible concept favors IgE-mediated reactivity towards allergens that enter the skin from the outside or through the blood. Microorganisms of the cutaneous flora also might represent a stimulus for allergic skin reactions. Abnormal bacterial skin colonization is a characteristic feature of AE. Staphylococcus aureus (S. aureus) is the most common pathogen. Binding to host cells involves special receptors, such as fibronectin or laminin. Specific IgE antibodies to S. aureus can be detected in the blood. Whereas the clinical relevance of anti-staphylococcal antibodies is still controversial, specific IgE antibodies to Pityrosporum species as well as positive type I prick test reactions to these yeasts seem to correlate with the intensity of eczematous lesions in the head and neck regions of patients with AE. Both antimicrobial and antifungal treatment has been shown helpful in some cases of AE.

Dermatitis, Atopic↗
PubMed1992

Differential increase in 12-HETE release and CD29/CD49f expression of platelets from normal donors and from patients with atopic dermatitis by Staphylococcus aureus.

The generation of the arachidonic acid-derived inflammatory mediator 12-hydroeicosatetraenoic acid (HETE) and the expression of CD29 as well as CD49f from unstimulated and stimulated platelets has been studied in patients with atopic dermatitis (AD) as well as in healthy volunteers. Heat-killed clinical isolates of Staphylococcus aureus served as stimuli. Unstimulated platelets from patients with AD produced higher amounts of 12-HETE compared to platelets from normal donors. The absolute 12-HETE release from platelets of patients with AD was significantly higher compared to the control group after stimulation with heat-killed S. aureus, whereas the relative increase remained. The expression of CD29 and CD49f on unstimulated platelets of patients with AD was markedly enhanced compared to platelets from normal donors. Stimulation with S. aureus led to similar results as to the CD29 expression on normal and atopic platelets or to a markedly higher expression of CD49f on platelets from normal donors. As compared to platelets from normal donors the CD49f expression on atopic platelets was slightly enhanced by S. aureus. Our data emphasize that platelets may play an important role in the pathogenesis of AD by an increased preactivation and by an enhanced responsiveness to S. aureus which colonizes permanently the skin of patients with AD.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1992

Effects of Staphylococcus aureus cell wall products (teichoic acid, peptidoglycan) and enterotoxin B on immunoglobulin (IgE, IgA, IgG) synthesis and CD23 expression in patients with atopic dermatitis.

The influence of staphylococcal cell wall products (teichoic acid, peptidoglycan) and enterotoxin B on peripheral blood lymphocytes (PBL) from patients with atopic dermatitis (AD) was investigated. The parameters studied were spontaneous and interleukin-inducible immunoglobulin (IgA, IgE, IgG) synthesis and CD23 expression. PBL from non-atopic donors served as controls. Teichoic acid and peptidoglycan induced an enhanced synthesis of IgA and IgG in normal donors. However, IgA and IgG synthesis in PBL from patients with AD was significantly suppressed by teichoic acid and enterotoxin B. The incubation of PBL from normal donors with enterotoxin B and interleukin-4 (IL-4) or IL-5 led to a significant suppression of IgA and IgG synthesis. Co-stimulation of PBL with teichoic acid or peptidoglycan and IL-4 led to a pronounced increase in IgE synthesis and CD23 expression in patients with AD. Our data indicate that cell wall products and toxins of staphylococci modulate the cytokine-dependent humoral immunity in patients with AD and may be responsible for allergic skin reactions in AD.

Antigens, Bacterial↗
PubMed1991

Characterization of allergenic components of rye and wheat flour (Secale, Triticum vulgaris) by western blot with sera of bakers: their effects on CD23 expression.

The allergenic components of water-soluble rye flour extract were studied by immunoblotting. Sera from 100 bakers were analyzed for their IgG, IgG4 and IgE binding pattern. Two allergens with molecular weights of 35 and 14 kD were detected. Previously, the major allergens of wheat flour extract were identified. The wheat flour components at a MW of 15/17 kD and the rye flour component at a MW of 14 kD were purified and isolated. The modulation of the low affinity receptor for IgE (Fc epsilon RII/CD23) on monocytes by separated allergenic components was studied. Depending on the allergen concentration the CD23 expression on isolated cells increased after stimulation with the rye flour component (MW 14 kD). The combined addition of the rye flour component (14 kD) with IL-4 induced a significant CD23 expression as compared to IL-4 alone.

Allergens↗
PubMed1991

Conversion of leukotriene A4 by neutrophils and platelets from patients with atopic dermatitis.

The generation of arachidonic acid-derived inflammatory mediators from unstimulated and stimulated neutrophils (PMN) and platelets in the presence of exogenous LTA4 has been studied in patients with atopic dermatitis (AD) as well as in healthy volunteers. PMN were stimulated with the interleukins IL-3, IL-8, C5a, and the Ca-ionophore A23187. In addition, NaF and thrombin were used to stimulate platelets. The release of leukotriene (LT)B4, 20-COOH- and 20-OH-LTB4, cysteinyl-leukotrienes and 12-HETE was measured. The proinflammatory mediator release from PMN and platelets of patients with AD was significantly higher as compared to the control group. The spontaneous conversion of LTA4 by PMN and platelets was markedly enhanced in patients with AD. Different results with receptor-specific and non-specific stimuli (Ca-ionophore A23187) in the presence of exogenous LTA4 were obtained. The results indicate a higher state of activation for enzymes involved in leukotriene formation. Furthermore, the production of 12-HETE by platelets from patients with AD was enhanced in unstimulated and stimulated cells. Our data emphasize that neutrophils and platelets may play an important role in the pathogenesis of AD by an increased responsiveness to receptor-specific stimuli and cell-cell interaction via LTA4.

Adolescent↗
PubMed1991

Staphylococcus aureus modifies the cytokine-induced immunoglobulin synthesis and CD23 expression in patients with atopic dermatitis.

The influence of Staphylococcus aureus on peripheral blood lymphocytes (PBL) of patients with atopic dermatitis (AD) was analysed. The parameters studied were spontaneous and interleukin-inducible immunoglobulin (IgA, IgE, IgG) synthesis, as well as CD23 expression. Various heat-killed, clinical isolates of S. aureus were analysed. PBL from non-atopic donors served as controls. The time-course of co-cultured PBL with S. aureus showed a dose-dependent increase in immunoglobulin (Ig) synthesis from PBL of normal donors, whereas the Ig synthesis of atopic cells was significantly depressed. Additional stimulation with interleukin-4 (IL-4) also led to a pronounced suppression of the IgE and IgA synthesis in normal donor cells, while the effect of S. aureus on PBL of atopic donors was not markedly affected by IL-4. Transwell cultures of bacteria separated from PBL by a semi-permeable membrane induced stimulation of IgA and IgE synthesis in patients with AD. The Ig synthesis in the control group was not altered. Co-stimulation of S. aureus and IL-4 in this system led to a suppression of IgA with cells of both atopic and normal donors. IgE synthesis from atopic PBL was significantly stimulated. The CD23 expression of atopic PBL was increased by S. aureus and IL-4. Our data indicate that S. aureus may modulate the cytokine-dependent humoral immunity in patients with AD and that chronic colonization of the skin may be responsible for allergic skin reactions in AD.

Antigens, Bacterial↗
PubMed1991

Interleukin-3, interleukin-8, FMLP and C5a enhance the release of leukotrienes from neutrophils of patients with atopic dermatitis.

The influence of the receptor-specific stimuli interleukin-3 (IL-3), interleukin-8 (IL-8), C5a and formyl-methionyl-leucyl-phenylalanine (FMLP) on the generation of arachidonic acid-derived inflammatory mediators from neutrophils (PMN) has been studied in patients with atopic dermatitis (AD) as well as in healthy, non-atopic volunteers. The release of leukotriene (LT)B4, the omega-oxidation products 20-COOH- and 20-OH-LTB4 and the cysteinyleukotriene LTC4 were measured by reverse-phase HPLC and radioimmunoassay. The incubation of neutrophils with these stimuli led to a significantly higher release of LTB4 and LTC4 in the AD group. The spontaneous leukotriene generation of PMN from patients with AD was on average threefold higher compared to the control group. C5a stimulated the release of LTB4 and its metabolites from atopic cells up to 9 ng in contrast to low amounts from non-atopic cells. Furthermore, FMLP distinctly enhanced the leukotriene release of neutrophils from patients with AD compared to unstimulated cells and to cells of normal donors. IL-3 and IL-8 also significantly stimulated the generation of LTB4 and LTC4 of PMN from atopic patients. Our data emphasize that neutrophils may play an important role in the pathogenesis of AD by an increased responsiveness to receptor-specific stimuli and further suggest that IL-3 and IL-8 influence the acute and chronic inflammatory reactions in patients with AD.

Cells, Cultured↗
PubMedDate not supplied

Staphylococcal enterotoxin B affects in vitro IgE synthesis, interferon-gamma, interleukin-4 and interleukin-5 production in atopic eczema.

Peripheral blood mononuclear cells from patients with atopic eczema (AE) stimulated with the 'superantigen' Staphylococcus enterotoxin B (SEB) secreted significantly more interleukin (IL)-4 and IL-5 as well as IgE, and markedly less interferon-gamma than those from healthy controls. Our results support the assumption that SEB produced by S. aureus colonizing the skin of patients with AE may induce expansion of IL-4- and IL-5-producing Th2 clones, leading to increased IgE synthesis and eosinophil activation.

Antigens, Bacterial↗