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Introduction: Allergic diseases represent a broad spectrum of high-prevalence, chronic conditions that remain underdiagnosed and undertreated. The aims of this interdisciplinary, questionnaire-based, non-interventional study were to identify and analyze potential barriers to clinical allergological care in Germany. Methods: All hospitals listed in the German hospital register involved in the treatment of allergological patients (n = 899) were invited to participate. The study yielded a response rate of 52.1% (n = 468). Results: Overall, 88.5% of clinics agreed that allergological care in Germany needs improvement, especially in terms of reimbursement for diagnostics and therapy. More than 80% of participating clinics reported that the decreased availability of test substances and the time-intensity of allergological testing represent relevant barriers. For dermatology and pulmonology, the former is the strongest barrier, while for pediatric and ENT clinics, time-intensity is regarded as the strongest barrier. The availability of good therapy and appropriate guidelines present no barriers to allergological care. Regarding the use of digital healthcare concepts, a very large majority of clinics (n = 352; 91.4%) do not offer video consultations or the use of health applications in patient care. Conclusion: In conclusion, we have identified several structural barriers to allergological care in Germany. Reimbursement and the use of digital healthcare concepts in German clinics providing allergological care need improvement. Based on the results of this study, there is an urgent need for researchers and policymakers to further investigate and support allergology departments in their clinical work and in their implementation of digital healthcare concepts.

Introduction: Environmental exposure to mites and fungi has been proposed to critically contribute to the development of IgE-mediated asthma. A common denominator of such organisms is chitin. Human chitinases have been reported to be upregulated by interleukin-13 secreted in the context of Th2-type immune responses and to induce asthma. We assessed whether chitin-containing components induced chitinases in an innate immune-dependent way and whether this results in bronchial hyperresponsiveness. Materials and Methods: Monocyte/macrophage cell lines were stimulated with chitin-containing or bacterial components in vitro. Chitinase activity in the supernatant and the expression of the chitotriosidase gene were measured by enzyme assay and quantitative PCR, respectively. Non-sensitized mice were stimulated with chitin-containing components intranasally, and a chitinase inhibitor was administered intraperitoneally. As markers for inflammation leukocytes were counted in the bronchoalveolar lavage (BAL) fluid, and airway hyperresponsiveness was assessed via methacholine challenge. Results: We found both whole chitin-containing dust mites as well as the fungal cell wall component zymosan A but not endotoxin-induced chitinase activity and chitotriosidase gene expression in vitro. The intranasal application of zymosan A into mice led to the induction of chitinase activity in the BAL fluid and to bronchial hyperresponsiveness, which could be reduced by applying the chitinase inhibitor allosamidin. Discussion: We propose that environmental exposure to mites and fungi leads to the induction of chitinase, which in turn favors the development of bronchial hyperreactivity in an IgE-independent manner.

Scope: Considering the increasing numbers of patients suffering from food allergy (FA) as well as the great variety of novel foods and food compositions, an unmet need exists for the development of preclinical approaches to characterize the allergenic potential of proteins. The aim of our study was to evaluate the allergenicity of different food allergens in a rat model. Methods: Brown Norway rats were sensitized to protein extracts (RuBisCO, apple, soy, peanut, garden pea) or ovalbumin (OVA) combined with Bordetella pertussis and aluminium hydroxide, followed by oral allergen challenges. Results: Allergen-specific serum immunoglobulin production and the proliferation of mononuclear cells from spleen confirmed sensitization. To assess functional alterations in the gut, intestinal permeability was measured, which increased in sensitized and challenged animals compared to non-sensitized controls. Allergens with high allergenic potential (peanut, OVA, soy) caused a stronger immunological response than allergens with low allergenic potential, such as RuBisCO and apple. Moreover, the immunological responses were reduced when using boiled instead of raw soy and pea proteins. Conclusion: This model mimics key features of FA and facilitates investigating the allergenicity of allergens in novel food or food compositions in vivo.

Background: The release of cytokines [interleukin-6 (IL-6), IL-8 and tumor necrosis factor-α (TNF-α)] by skin cells is involved in the pathogenesis of atopic dermatitis (AD). Objective: To evaluate the effect of low-dose cyclosporin A (CyA) on clinical symptoms and cytokine secretion in severe pediatric AD. Methods: Ten children with severe AD (SCORAD index >50) were treated for 8 weeks with CyA. The initial dose of 2.5 mg/kg/day was titrated to a maximum of 5 mg/kg/day until a SCORAD reduction of ≧35% was achieved (‘treatment response’). After stopping CyA all patients entered a 4-week follow-up period. Cytokine secretion (IL-6, IL-8 and TNF-α) from patients’ PBMC was assessed by ELISA before and after CyA treatment and was compared with 18 healthy nonatopic controls. Only the data of patients, who responded to CyA and did not experience a relapse during the follow-up period, were evaluated for this paper. Results: Seven patients responded to CyA without relapse during the follow-up period. The median SCORAD index in these patients improved from 71 at baseline to 22 after CyA treatment (p < 0.001). AD patients’ PBMC produced more IL-6, IL-8 and TNF-α than PBMC of controls. Suppression of IL-6 (p < 0.05) and IL-8 (p < 0.05) production was observed after CyA treatment. TNF-α levels were unchanged by CyA in all patients. Conclusions: The reduction in severity of pediatric AD with CyA is associated with decreased production of IL-6 and IL-8, but not TNF-α by PBMC.

Increased production of interleukin (IL)–4 and IL–5 by T–helper cells may be pivotal for the induction and regulation of allergic diseases. We have studied the role of IL–4 and IL–5 in the development of eosinophilic airway inflammation (AI) and airway hyperresponsiveness (AHR) in a mouse model of allergen–induced bronchial asthma. Utilizing different modes of sensitization, we delineated the importance of IL–5–mediated eosinophilic airway infiltration for the development of in vitro and in vivo AHR and demonstrated the inhibition of airway inflammation and AHR by anti–IL–5 antibody treatment. Studies in IL–4– and IL–5 deficient mice revealed the importance of both cytokines for the induction of AI and AHR independently from the production of allergen–specific IgE, and indicated these cytokines as potential targets in novel approaches in the treatment of asthma.

This review evaluates the role of IL–5 and IL–5–mediated eosinophil airway infiltration in the development of allergen–driven airway hyperresponsiveness. It discusses the structure and function of IL–5 and its receptor and the mechanisms of IL–5–triggered eosinophil accumulation and inflammation of the airways. New research data from murine models of airway inflammation and hyperresponsiveness utilizing different modes of sensitization to allergen and anti–IL–5 antibody or IL–5–deficient knock–out mice underscore the outstanding role of this cytokine in the pathogenesis of bronchial asthma. This review identifies possible directions for future treatment of airway hyperresponsiveness and concludes that targeting IL–5–driven inflammatory responses may be most beneficial for a novel therapy in bronchial asthma.