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Background: Chromosomal region 5q31 harbours a number of genes associated with atopic phenotypes, for example the genes coding for interleukin (IL) 4, IL 13 and the β[sub2]-adrenoreceptor. A new gene within this region was identified only very recently. The encoded protein-uteroglobin-related protein 1 A(UGRP1)--is thought to act as an anti-inflammatory agent and is mainly expressed in the lung and trachea. The functional promoter polymorphism A-112G in UGRP1 was shown to be associated with bronchial asthma in a Japanese population. We were thus interested in finding out whether the polymorphism so far identified or others within UGRP1 were associated with bronchial asthma in a German Caucasian population. Methods: We performed direct genomic sequencing of the promoter and coding region of UGRP1 in 15 asthmatic children and 15 controls. The identified polymorphisms were genotyped by means of RFLP. Statistical analysis was performed with the Armitage trend test. Results: We identified 5 non-coding variants, 4 of which being described for the first time. Three polymorphisms were common and typed in 182 asthmatic children and 270 controls. None of the polymorphisms were associated with bronchial asthma in our population. Conclusions: We conclude from our data that UGRP1 doest not play a major role in the development of bronchial asthma in our Caucasian population. [ABSTRACT FROM AUTHOR]

Background: β–Lactoglobulin (BLG) represents one of the major allergens causing cow’s milk allergy (CMA) – a disease with a wide spectrum of clinical symptoms. The aim of this study was to evaluate sequential B cell epitopes of BLG by the Pin–ELISA method. Furthermore, we wanted to investigate a possible association of the IgE recognition patterns in sera of patients with BLG sensitization and the type of clinical reactions following contact with cow’s milk. Methods: Overlapping sequential decapeptides corresponding to the amino acid sequence of BLG were used in Pin–ELISAs specific for human IgE. Tested sera were from 14 individuals with CMA, 8 of them with a history of immediate systemic reactions and 6 with delayed skin reactions following contact with cow’s milk. All of them showed specific IgE antibodies to BLG in the CAP–RAST. Control sera were from 5 healthy nonallergic individuals. Results: All sera from BLG–sensitized individuals showed IgE binding with one region of BLG corresponding to amino acids 95–113. Furthermore, individual sera showed reactions with two further regions, 12–27 and 124–135. Inhibition of IgE binding to BLG with one soluble synthetic peptide confirmed the major epitope. No differences were found in the B cell epitope recognition pattern to BLG in the two groups of patients with CMA, characterized by acute systemic or delayed skin reactions. Conclusions: Using IgE Pin–ELISAs we were able to confirm previously described sequential B cell epitopes of BLG. However, the recognition pattern of one of the major cow’s milk allergens is not predictive of the clinical type of reaction. [ABSTRACT FROM AUTHOR]

Background: Recently linkage and association of the chromosomal region 16p12–11 with enhanced IgE responsiveness have been shown. The gene coding for CD43 (sialophorin) has been localized to this region. Sialophorin represents a major sialoglycoprotein on the surface of human lymphocytes, monocytes and granulocytes. It is supposed to play an important role in human mast cell, T– and B–cell regulation and activation and has been described in connection with immunodeficiency diseases such as the Wiskott–Aldrich syndrome. Therefore, it can be designated as a candidate gene for atopy. Methods: Using SSCP analysis and direct genomic sequencing, polymorphisms in the CD43 gene have been looked for and their association with atopy has been tested in a population of 260 largely atopic children and young adults. Results: Three common polymorphisms in the coding part of the CD43 gene were found. Two of them are leading to amino acid exchanges, one from argine to cysteine at amino acid position 337 of the mature gene product and one from leucine to phenylalanine at amino acid position 341. Subsequent association studies revealed no obvious influence of R337C or L341F on IgE regulation (p = 0.47 and 0.43), neither in a cognate nor in an uncognate fashion. Conclusion: We conclude that CD43 polymorphisms are unlikely to account for the observed linkage effect at 16p12–11. Whether the polymorphisms R337C and L341F adjacent to phosphorylation sites in the intracellular region of the protein alter the normal functioning of CD43 remains to be elucidated. [ABSTRACT FROM AUTHOR]