Pichler U.,Christian Doppler Laboratory |
Hauser M.,Christian Doppler Laboratory |
Wolf M.,Christian Doppler Laboratory |
Bernardi M.L.,Centers for Molecular Allergology |
And 15 more authors.
PLoS ONE | Year: 2015
Background Pollen released by allergenic members of the botanically unrelated families of Asteraceae and Cupressaceae represent potent elicitors of respiratory allergies in regions where these plants are present. As main allergen sources the Asteraceae species ragweed and mugwort, as well as the Cupressaceae species, cypress, mountain cedar, and Japanese cedar have been identified. The major allergens of all species belong to the pectate lyase enzyme family. Thus, we thought to investigate cross-reactivity pattern as well as sensitization capacities of pectate lyase pollen allergens in cohorts from distinct geographic regions. Methods The clinically relevant pectate lyase pollen allergens Amb a 1, Art v 6, Cup a 1, Jun a 1, and Cry j 1 were purified from aqueous pollen extracts, and patients' sensitization pattern of cohorts from Austria, Canada, Italy, and Japan were determined by IgE ELISA and cross-inhibition experiments. Moreover, we performed microarray experiments and established a mouse model of sensitization. Results In ELISA and ELISA inhibition experiments specific sensitization pattern were discovered for each geographic region, which reflected the natural allergen exposure of the patients. We found significant cross-reactivity within Asteraceae and Cupressaceae pectate lyase pollen allergens, which was however limited between the orders. Animal experiments showed that immunization with Asteraceae allergens mainly induced antibodies reactive within the order, the same was observed for the Cupressaceae allergens. Cross-reactivity between orders was minimal. Moreover, Amb a 1, Art v 6, and Cry j 1 showed in general higher immunogenicity. Conclusion We could cluster pectate lyase allergens in four categories, Amb a 1, Art v 6, Cup a 1/Jun a 1, and Cry j 1, respectively, at which each category has the potential to sensitize predisposed individuals. The sensitization pattern of different cohorts correlated with pollen exposure, which should be considered for future allergy diagnosis and therapy. © 2015 Pichler et al. Source
Cramer C.,Iuf Institute For Umweltmedizinische Forschung |
Link E.,Iuf Institute For Umweltmedizinische Forschung |
Horster M.,Iuf Institute For Umweltmedizinische Forschung |
Koletzko S.,Ludwig Maximilians University of Munich |
And 14 more authors.
Journal of Allergy and Clinical Immunology | Year: 2010
Background: Several studies showed a protective effect of elder siblings on eczema development, which is in line with the hygiene hypothesis. However, findings are not consistent, and there might exist different causal pathways for the development of eczema. Especially barrier disturbances as found in children with mutations in the filaggrin gene (FLG) seem to play an important role. Objectives: To investigate the interaction between FLG mutations and the presence of elder siblings on the development of eczema in 2 independent birth cohorts. Methods: We used data from 2 German birth cohorts (LISAplus, GINIplus) up to the age of 6 years. Genotyping for FLG mutations (R501X, 2282del4) was performed in 1039 (LISAplus) and 1828 (GINIplus) children. Data on eczema (diagnosis and symptoms) and elder siblings were obtained by parental questionnaires. The association among eczema, FLG mutations, and elder siblings was analyzed longitudinally by using generalized estimating equations. Results: We found no protective effect of elder siblings on eczema development. On the contrary, children with FLG mutations had a significantly higher risk for eczema if they had elder siblings. Attending day care centers lessened this effect. After excluding 303 children who attended early day care, the odds ratio for interaction between FLG mutations and elder siblings was 3.27 (95% CI, 1.14-9.36) in LISAplus and 2.41 (95% CI, 1.06-5.48) in GINIplus. Conclusion: Our findings did not confirm a protective sibling effect. The prevalence of eczema in children with filaggrin deficiency was higher if elder siblings were present. Our results give evidence for complex skin-driven pathogenic mechanisms that might be different depending on children's genetic backgrounds. © 2010 American Academy of Allergy, Asthma & Immunology. Source
Eyerich K.,Center for Allergy and Environment |
Eyerich S.,Center for Allergy and Environment |
Hiller J.,Center for Allergy and Environment |
Behrendt H.,Center for Allergy and Environment |
And 2 more authors.
European Journal of Dermatology | Year: 2010
Chronic mucocutaneous candidiasis (CMC) defines a heterogeneous group of orphan and inherited syndromes characterised by chronic and recurrent infections of the skin and mucosa with the yeast Candida. Increasing evidence suggests that this inefficient defence against Candida species is reflected by a DC/T cell defect which results in an impaired Th17 and Th1 immune response and, consecutively, a failed immune instruction of tissue cells. Little is known about the incidence and prognosis of CMC. Clinically, the main complications are debilitating hands (Candida granuloma) and oesophageal stricture with potential mal-digestion/-absorption. Furthermore, the chronic infections are likely a risk factor for the development of squamous cell carcinoma. Since resistance to anti-mycotic drugs evolves rapidly, efficient and flexible therapeutic management is essential for CMC patients. Source
Darsow U.,TU Munich |
Darsow U.,Center for Allergy and Environment |
Wollenberg A.,Ludwig Maximilians University of Munich |
Simon D.,University of Bern |
And 12 more authors.
World Allergy Organization Journal | Year: 2013
Difficult to control atopic dermatitis (AD) presents a therapeutic challenge and often requires combinations of topical and systemic treatment. Anti-inflammatory treatment of severe AD most commonly includes topical glucocorticosteroids and topical calcineurin antagonists used for exacerbation management and more recently for proactive therapy in selected cases. Topical corticosteroids remain the mainstay of therapy, the topical calcineurin inhibitors tacrolimus and pimecrolimus are preferred in certain locations. Systemic anti-inflammatory treatment is an option for severe refractory cases. Microbial colonization and superinfection contribute to disease exacerbation and thus justify additional antimicrobial/antiseptic treatment. Systemic antihistamines (H1) may relieve pruritus but do not have sufficient effect on eczema. Adjuvant therapy includes UV irradiation preferably of UVA1 wavelength. "Eczema school" educational programs have been proven to be helpful. © 2013 Darsow et al.; licensee BioMed Central Ltd. Source
Darsow U.,Center for Allergy and Environment |
Darsow U.,TU Munich |
Fedorov M.,Center for Allergy and Environment |
Fedorov M.,TU Munich |
And 8 more authors.
Contact Dermatitis | Year: 2012
Background. Nickel is a frequently detected cause of allergic contact dermatitis. Ingestion of nickel may lead to flares of nickel contact dermatitis. Methods. We examined nickel excretion in the urine of 164 female patients with and without nickel contact dermatitis. The associations between age, atopic dermatitis, nickel contact dermatitis and nickel exposure through nutrition (e.g. dietary supplements) and by patch tests were investigated prospectively. Nickel was measured with atomic absorption spectrometry with two different standardized methods. Results. A nickel detection limit of 0.2 μg/l was exceeded by all samples. The 95th percentiles of urine nickel concentration were 3.77 μg/l (age 18-30 years) and 3.98 μg/l (age 31-46 years). Bivariate analyses pointed to significantly increased nickel excretion with increasing age, ingestion of dietary supplements, drinking of stagnant tap water, and consumption of nickel-rich food. In the multivariate analysis, age and dietary supplements remained significant predictors of high nickel excretion. A non-significant increase in the median concentration of nickel was observed after the administration of conventional nickel patch tests. Patients with atopic eczema showed urine nickel concentrations similar to those in non-atopic controls. Conclusions. The 95th percentile of nickel excretion in our study population markedly exceeded the actual reference value of 3 μg/l. Age and consumption of dietary supplements are the most important predictors. The use of stagnant tap water and consumption of nickel-rich food contribute to the total load. These factors should be explicitly mentioned when allergic patients on a low-nickel diet are counselled. In contrast, existing nickel contact sensitization was not more frequent in subjects with higher nickel excretion. Nickel patch testing may cause transient minor systemic nickel exposure. The findings of this study extend our understanding and management of factors associated with nickel allergy. © 2012 John Wiley & Sons A/S. Source