Elisabeth André

Ludwig-Maximilian-University of Munich, München, Bavaria, Germany

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Publications (5)40.28 Total impact

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    ABSTRACT: To identify genome regions linked to serum vitamin D metabolites we analyzed 25-OH-D(3) and 1,25-(OH)(2)-D(3) levels from 947 participants of a family study recruited for asthma. From these individuals data were available from a previous genome scan that included 364 autosomal microsatellite marker. 25-OH-D(3) levels showed a heritability of 80% in these families while 1,25-(OH)(2)-D(3) reached only 30%. Genome-wide linkage using variance component analysis showed increased LOD scores for 25-OH-D(3) at marker D1S2815 (unadjusted LOD 2.9), D2S2153 (LOD 3.4), D5S2017 (LOD 2.5), D6S260 (LOD 2.1) and D17S1824 (2.5). In contrast, the maximum LOD score for 1,25-(OH)(2)-D(3) level was only 1.2 at marker D17S926. We conclude that only 25-OH-D(3) serum levels are under genetic control where several genes are involved. The lead linkage region does not code for enzymes already known in the metabolic pathway of vitamin D and may therefore contain further genes relevant to the regulation of vitamin D serum levels.
    The Journal of Steroid Biochemistry and Molecular Biology 04/2007; 103(3-5):799-802. · 3.98 Impact Factor
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    ABSTRACT: High levels of particulate matter in ambient air are associated with increased respiratory and cardiovascular health problems. It has been hypothesised that it is the ultrafine particle fraction (diameter <100 nm) that is largely responsible for these effects. To evaluate the associated mechanisms on a molecular level, the current authors applied an expression profiling approach. Healthy mice were exposed to either ultrafine carbon particles (UFCPs; mass concentration 380 microg x m(-3)) or filtered air for 4 and 24 h. Histology of the lungs did not indicate any pathomorphological changes after inhalation. Examination of the bronchoalveolar lavage fluid revealed a small increase in polymorphonuclear cell number (ranging 0.6-1%) after UFCP inhalation, compared with clean air controls, suggesting a minor inflammatory response. However, DNA microarray profile analysis revealed a clearly biphasic response to particle exposure. After 4 h of inhalation, mainly heat shock proteins were induced, whereas after 24 h, different immunomodulatory proteins (osteopontin, galectin-3 and lipocalin-2) were upregulated in alveolar macrophages and septal cells. In conclusion, these data indicate that inhalation of ultrafine carbon particles triggers a biphasic pro-inflammatory process in the lung, involving the activation of macrophages and the upregulation of immunomodulatory proteins.
    European Respiratory Journal 09/2006; 28(2):275-85. · 6.36 Impact Factor
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    ABSTRACT: The vitamin D prophylaxis of rickets in pregnant women and newborns may play a role in early allergic sensitization. We now asked if an already diseased population may have inherited genetic variants in the vitamin D turnover or signalling pathway. Serum levels of calcidiol (25-OH-D3) and calcitriol (1,25-(OH)2-D3) were retrospectively assessed in 872 participants of the German Asthma Family Study. 96 DNA single base variants in 13 different genes were genotyped with MALDI-TOF and a bead array system. At least one positive SNP with a TDT of p < 0.05 for asthma or total IgE and calcidiol or calcitriol was seen in IL10, GC, IL12B, CYP2R1, IL4R, and CYP24A1. Consistent strong genotypic association could not be observed. Haplotype association were found only for CYP24A1, the main calcidiol degrading enzyme, where a frequent 5-point-haplotype was associated with asthma (p = 0.00063), total IgE (p = 0.0014), calcidiol (p = 0.0043) and calcitriol (p = 0.0046). Genetic analysis of biological pathways seem to be a promising approach where this may be a first entry point into effects of a polygenic inherited vitamin D sensitivity that may affect also other metabolic, immunological and cancerous diseases.
    Respiratory research 01/2006; 7:60. · 3.64 Impact Factor
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    ABSTRACT: The space and time distribution of risk factors for allergic diseases may provide insights into disease mechanisms. Allergy is believed to vary by month of birth, but multinational studies taking into account latitude have not been conducted. A questionnaire was distributed in 54 centres to a representative sample of 20- to 44-y-old men and women mainly in Europe but also including regions in North Africa, India, North America, Australia, and New Zealand. Data from 200,682 participants were analyzed. The median prevalence of allergic rhinitis was 22%, with a substantial variation across centres. Overall, allergic rhinitis decreased with geographical latitude, but there were many exceptions. No increase in prevalence during certain winters could be observed. Also, no altered risk by birth month was found, except borderline reduced risks in September and October. Effect estimates obtained by a multivariate analysis of total and specific IgE values in 18,085 individuals also excluded major birth month effects and confirmed the independent effect of language grouping. Neither time point of first exposure to certain allergens nor early infections during winter months seems to be a major factor for adult allergy. Although there might be effects of climate or environmental UV exposure by latitude, influences within language groups seem to be more important, reflecting so far unknown genetic or cultural risk factors.
    PLoS Medicine 11/2005; 2(10):e294. · 15.25 Impact Factor
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    ABSTRACT: The interleukin-1 cluster on human chromosome 2q12-2q14 harbors various promising candidate genes for asthma and other inflammatory diseases. We conducted a systematic association study with single-nucleotide polymorphisms (SNPs) located in candidate genes situated in this cluster. Single-marker, two-locus and three-locus haplotype analysis of SNPs yielded several significant results (p < 0.05-0.0021) for the human IL1RN gene encoding the IL-1 receptor antagonist protein, an antiinflammatory cytokine that plays an important role in maintaining the balance between inflammatory and antiinflammatory cytokines. These findings were replicated and confirmed in an independent Italian family sample in which significant, although weaker, association with asthma was detected. A sequencing approach to the coding region of the human IL1RN gene revealed additional DNA variants, from which a selection was also associated with the disease in German and Italian samples. Calculation of the linkage disequilibrium for the human IL1RN gene showed strong linkage disequilibrium for nearly all analyzed SNPs. Further haplotype analysis indicated that six SNPs are sufficient for tagging all haplotypes with a prevalence of more than 1%. The most frequent haplotype constructed from these SNPs was 1.4-fold overtransmitted in the German family sample.
    American Journal of Respiratory and Critical Care Medicine 06/2004; 169(11):1217-23. · 11.04 Impact Factor