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Bettina Wedi

Publications and source records attributed to Bettina Wedi.

8 recordsLinked to original sources
PubMed2005

Brain-derived neurotrophic factor is increased in atopic dermatitis and modulates eosinophil functions compared with that seen in nonatopic subjects.

BACKGROUND: Recently, the pivotal role of brain-derived neurotrophic factor (BDNF) has been described in allergic asthma. However, the role of this neurotrophin in atopic dermatitis (AD) still remains unknown. OBJECTIVE: The aim of this study was to investigate the functional role of BDNF on eosinophils and to assess BDNF levels in patients with AD and nonatopic control subjects. Methods p75 Neurotrophin receptor and tyrosine kinase B receptor expression was demonstrated by using FACS analysis and immunohistochemistry. BDNF levels were assessed with ELISA and FACS analysis. Chemotactic activity (modified Boyden chamber assay), eosinophil cationic protein release (fluoroenzyme immunoassay), respiratory burst (lucigenin-dependent chemiluminescence), and apoptosis (Nicoletti protocol and Annexin-V method) assays were used to assess BDNF functional activity. RESULTS: BDNF levels were increased in serum, plasma, eosinophils, and supernatants of stimulated eosinophils from patients with AD compared with levels seen in nonatopic control subjects ( P < .05-.001). In addition, p75 neurotrophin receptor and tyrosine kinase B expression was higher on eosinophils from patients with AD compared with that seen on eosinophils from nonatopic control subjects ( P < .05-.001). Eosinophil apoptosis was inhibited by BDNF ( P < .05-.01) and chemotactic index was increased ( P < .001) in BDNF-stimulated eosinophils from patients with AD, whereas this effect was not shown in eosinophils from nonatopic control subjects. However, no response of BDNF through the release of eosinophil cationic protein or reactive oxygen species was found. CONCLUSION: This study provides the first evidence for a functional role of BDNF on eosinophils from patients with AD, probably mediated by an increased expression of BDNF receptors compared with that seen in nonatopic control subjects. In addition, higher intracellular, serum, and plasma BDNF levels, as well as the release of BDNF by eosinophils, underline the particular importance of BDNF in patients with AD, pointing to new pathophysiologic aspects of this chronic inflammatory skin disease.

Apoptosis↗
PubMed2004

Chronic urticaria and infections.

PURPOSE OF REVIEW: The pathogenesis of chronic urticaria is multifactorial and a specific treatment is lacking. In acute urticaria there is no doubt of a causal relationship with infections and all chronic urticaria must start as the acute form. However, in the chronic form a primary role for infection is controversial, although it is undeniable that concurrent infections exacerbate the condition. This is the first English language review based on a detailed analysis of current peer-reviewed publications dealing with infections and chronic urticaria. RECENT FINDINGS: In chronic urticaria there is a lot of evidence for different infections, but randomized controlled trials are missing. The prevalence of infections is not increased but in susceptible patients the immune response may lead to the development of chronic urticaria. Interestingly, there is evidence for an infection-associated autoreactive response at least in the subgroup with a positive autologous serum skin test. A variety of mechanisms have been invoked to explain these observations, including molecular mimicry. SUMMARY: Actually the arguments for an important role of underlying causal infections in chronic urticaria are weak, from an evidence-based viewpoint, but there are data suggesting a link. Moreover, an association with underlying or precipitating infectious causes is difficult to establish because there is no possibility for challenge and the number of other urticarial triggers is vast. For the future it will be necessary to reveal the link between urticaria, autoreactivity, non-immunoglobulin E-mediated hypersensitivity reactions and infections to find attractive and specific therapeutic interventions for urticarial symptomatology.

Acute Disease↗
PubMed2002

Staphylococcal exotoxins exert proinflammatory effects through inhibition of eosinophil apoptosis, increased surface antigen expression (CD11b, CD45, CD54, and CD69), and enhanced cytokine-activated oxidative burst, thereby triggering allergic inflammatory reactions.

BACKGROUND: Staphylococcus aureus colonization of the skin represents a potent trigger factor of atopic dermatitis. Our previous studies demonstrated that in atopic dermatitis eosinophil apoptosis is significantly delayed. OBJECTIVE: We sought to investigate the effect of staphylococcal exotoxins (SETs) on eosinophil apoptosis and functional activities. METHODS: Apoptotic eosinophils were investigated by determining their hypodiploid DNA peak. Eosinophil surface-antigen expression and intracellular production of hydrogen peroxide were assessed by means of flow cytometric analysis and respiratory burst by lucigenin-dependent chemiluminescence. RESULTS: The SETs SEA, SEB, SEC, and toxic shock syndrome toxin 1 significantly inhibited eosinophil apoptosis in a manner comparable with that of high concentrations of IL-3. The LPS inhibitor polymyxin B was found to significantly inhibit LPS-mediated, but not SET-mediated, inhibition of apoptosis. Neither SETs nor LPS was able to modulate eosinophil surface expression of CD9, CD11a, CD16, CD40, CD44, or CD63. However, 24- and 48-hour incubation with all SETs, but not with LPS, significantly upregulated expression of CD11b and CD45 in a manner similar to that of IL-3, whereas dexamethasone induced a downregulation. Moreover, all SETs resulted in a significant upregulation of CD54 after 24 hours but not after 48 hours. Interestingly, CD69 was upregulated by means of IL-3 and SEB only. Neither direct stimulation of eosinophils nor 24-hour incubation with SETs or stimulation with SETs after a 24-hour prestimulation with IL-3, IL-5, or GM-CSF resulted in a significant extracellular production of reactive oxygen species or in a significant production of intracellular hydrogen peroxide. However, SEB and toxic shock syndrome toxin 1 were able to enhance cytokine-induced respiratory burst. CONCLUSION: Taken together, our data demonstrate that SETs may modulate the course of the allergic inflammatory response through modulation of potent eosinophil effector functions. This may be of particular importance in atopic dermatitis, in which the skin is regularly colonized with SET-producing S aureus.

Antigens, CD↗
PubMed2002

Helicobacter pylori infection in skin diseases: a critical appraisal.

More than 50% of the human population have long-term Helicobacter pylori infection, causing, in some cases, severe diseases such as peptic ulcers and stomach cancer. In the last few years several extra-gastrointestinal disorders have been associated with H. pylori infection. This review summarized the current medical literature, identified through hand searching and MEDLINE research, including our own studies, with regard to H. pylori and skin diseases. From the literature it can be seen that the role of H. pylori in skin diseases is still a controversial subject. Randomized controlled trials with adequate masking and sample sizes are still lacking. The best evidence comes from studies investigating chronic urticaria in which chronic urticaria disappeared in many patients with H. pylori infection after careful eradication of the H. pylori. Moreover, there are promising recent reports of beneficial H. pylori eradication in Behçet's disease, pruritus cutaneus, prurigo chronica, prurigo nodularis and in some patients with lichen planus, but not in rosacea or psoriasis. Before any conclusions with respect to other skin diseases such as atopic dermatitis, Schoenlein-Henoch Purpura, Sweet's syndrome, Sjögren syndrome or systemic sclerosis may be drawn, additional randomized, double-blinded and placebo-controlled studies including adequate diagnostic schedules, sufficient eradication treatment protocols, confirmation of eradication and adequate control groups are needed. The cutaneous pathology of H. pylori is far from being clear, but it is speculated that the systemic effects may involve increased mucosal permeability to alimentary antigens, immunomodulation, an autoimmune mechanism or the impairment of vascular integrity.

Amoxicillin↗