Mechanisms of AllergyAssociation between polymorphisms in caspase recruitment domain containing protein 15 and allergy in two German populations☆,☆☆
Section snippets
Subjects
Between 1995 and 1996, a cross-sectional study was conducted in Munich, West Germany, and Dresden, East Germany, to assess the prevalence of asthma and allergies in schoolchildren aged 9 to 11 years.9 Parental questionnaires for self-completion were sent through the schools to the families. Children underwent skin prick testing, pulmonary function testing, and bronchial challenge with hyperosmolar saline (4.5%) at their schools. Blood was collected for serum IgE measurements and DNA extraction.
Results
All available blood samples in Munich (N = 1161) and a random sample of 50% of all available blood samples in Dresden (N = 711) were genotyped for the 3 SNPs in the CARD15 gene previously reported to be associated with Crohn's disease.5, 6, 7 No selection bias could be detected between children genotyped for this study and those who were not (Tables I and II). Furthermore, no significant difference was present between children genotyped for CARD15 polymorphisms in Munich and Dresden (Table I,
Discussion
In this study we showed that 3 polymorphisms in the CARD15 gene previously related to the development of Crohn's disease are also associated with atopic diseases. This observation was consistent in 2 population samples from East and West Germany. The strongest association was observed with allergic rhinitis, in which 2 CARD15 polymorphisms independently increased the risk to develop the disease by 2- to 3-fold. From these results we conclude that even though the frequency of CARD15
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2020, Biochemical and Biophysical Research CommunicationsCitation Excerpt :Impairments of NLR signaling are recognized risk factors for several chronic inflammatory diseases, including atopic dermatitis [13–15]. NOD1 and NOD2 polymorphisms have been related to elevated IgE levels and atopic dermatitis [17,18]. In addition, skin lesions of atopic dermatitis have been reported to exhibit decreased innate immune responses, including expression of β-defensin and IL-8 [19–21].
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Supported by German Ministry of Education and Research (BMBF)/National Genome Research Network (NGFN): Research grant BMBF 01GS 0122 (NGFN).
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Reprint requests: Michael Kabesch, MD, Children's University Hospital, Ludwig Maximilians University Munich, Lindwurmstrasse 4, D-80337 München, Germany.