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During the last decades, the prevalence of allergy has dramatically increased. Allergen-specific immunotherapy is the only currently available medical intervention that has the potential to affect the natural course of the disease, but there are still many questions and unmet needs hindering its widespread use to fulfill its treatment potential and maximize its benefits for the society. To provide a comprehensive phenome-wide overview in sublingual immunotherapy, using ragweed allergy as a target, we planned and carried out a longitudinal, prospective, observational, open-label study (DesensIT). In this paper we present challenges of using deep and comprehensive phenotypes embracing biological, clinical and patient-reported outcomes in allergen-specific immunotherapy and show how we designed the DesensIT project to optimize data collection, processing and evaluation.

Air pollution and subsequent increased oxidative stress have long been recognized as contributing factors for asthma phenotypes. Individual susceptibility to oxidative stress is determined by genetic variations of the antioxidant defence system. In this study, we analysed the association between environmental nitrogen dioxide (NO(2)) exposure and single nucleotide polymorphisms (SNP) in NFE2L2 and KEAP1 genes and their common impact on asthma risk. We genotyped 12 SNPs in a case-control study of 307 patients diagnosed with asthma and 344 controls. NO(2) concentration was collected from the period preceding the development of asthma symptoms. Multiple logistic regression was applied to evaluate the effects of the studied genetic variations on asthma outcomes in interaction with NO(2) exposure. Our data showed that genotypes of rs2588882 and rs6721961 in the regulatory regions of the NFE2L2 gene were inversely associated with infection-induced asthma (odds ratio (OR) = 0.290, p = 0.0015, and OR = 0.437, p = 0.007, respectively). Furthermore, case-only analyses revealed significant differences for these SNPs between asthma patients that lived in modestly or highly polluted environment (OR = 0.43 (0.23-0.82), p = 0.01, and OR = 0.51, p = 0.02, respectively, in a dominant model). In conclusion, our results throw some new light upon the impact of NFE2L2 polymorphisms on infection-induced asthma risk and their effect in gene-environment interactions.

The authors have summed up the survey results for children with asthma below 14 years of age participating in the Hunair II. surveillance program. This program proves the efficiency of montelucast 5mg treatment in cases of childhood asthma bronchiale. The 255 patients participating in the survey have received 5 mg montelucast therapy for 8 weeks. During the surveillance period they have used questionnaires to record the change of day and night symptoms, decrease of different restrictions and the quantity change of long- and short-acting beta agonists and inhaled steroids. The use of short-acting agonists decreased from 5 inhalations to 1 in 4 weeks. During the leukotriene antagonist montelucast treatment according to symptom scores 61% of the patients have experienced improvements after the 4th week, 80% after the 8th week. To sum up all the survey results--after the 8th week of treatment the daytime restrictions in the everyday lives of children with asthma have decreased by 88.1%, nighttime restrictions by 80.1%. After the 2nd month of the HUNAIR II. surveillance program it could be deduced that montelucast 5 mg therapy used in child populations less then 14 years of age with asthma has proven useful.