Evaluation of the CD14/-260 polymorphism and house dust endotoxin exposure in the Barbados Asthma Genetics Study

Zambelli-Weiner, April; Ehrlich, Eva; Stockton, M.; Grant, Audrey V.; Zhang, Shu; Levett, Paul N.; Beaty, Terri H.; Barnes, Kathleen C.

doi:10.1016/j.jaci.2005.03.001

Cited by 140 publications

(123 citation statements)

References 36 publications

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“…The average age (6 SD) of offspring with asthma was 21.8 6 13.23 years in the African Caribbean families, 14.6 6 7.7 years in the African American families, 20.0 6 10.8 years in the European American families, 23.27 6 17.03 years in the Brazilian families, and 17.54 6 10.1 years in the Colombian families. Among African Caribbean, African American, and European American family members (745, 368, and 494 individuals, respectively), means of tIgE concentrations were similar to those described previously (23,29,30). In general, tIgE levels were significantly different between founders in each pair of populations except for the comparison of African American and European American populations (P 5 0.161).…”

Section: Demographic Characteristicssupporting

confidence: 82%

Gene Encoding Duffy Antigen/Receptor for Chemokines Is Associated with Asthma and IgE in Three Populations

Vergara¹,

Tsai²,

Grant³

et al. 2008

Am J Respir Crit Care Med

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Rationale: Asthma prevalence and severity are high among underserved minorities, including those of African descent. The Duffy antigen/receptor for chemokines is the receptor for Plasmodium vivax on erythrocytes and functions as a chemokine-clearing receptor. Unlike European populations, decreased expression of the receptor on erythrocytes is common among populations of African descent, and results from a functional T-46C polymorphism (rs2814778) in the promoter. This variant provides an evolutionary advantage in malaria-endemic regions, because Duffy antigen/receptor for chemokines-negative erythrocytes are more resistant to infection by P. vivax. Objectives: To determine the role of the rs2814778 polymorphism in asthma and atopy as measured by total serum IgE levels among four populations of African descent (African Caribbean, African American, Brazilian, and Colombian) and a European American population. Methods: Family-based association tests were performed in each of the five populations to test for association between the rs2814778 polymorphism and asthma or total IgE concentration. Measurements and Main Results: Asthma was significantly associated with the rs2814778 polymorphism in the African Caribbean, Colombian, and Brazilian families (P , 0.05). High total IgE levels were associated with this variant in African Caribbean and Colombian families (P , 0.05). The variant allele was not polymorphic among European Americans. Conclusions: Susceptibility to asthma and atopy among certain populations of African descent is influenced by a functional polymorphism in the gene encoding Duffy antigen/receptor for chemokines. This genetic variant, which confers resistance to malarial parasitic infection, may also partially explain ethnic differences in morbidity of asthma.

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Section: Demographic Characteristicssupporting

confidence: 82%

Gene Encoding Duffy Antigen/Receptor for Chemokines Is Associated with Asthma and IgE in Three Populations

Vergara¹,

Tsai²,

Grant³

et al. 2008

Am J Respir Crit Care Med

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“…[19][20][21][22][23][24] Differences in the frequency of these polymorphisms by both race and ethnicity have also been described. 23,[25][26][27] The relative contribution of these genotypic differences to asthma disparities is currently unknown.…”

Section: Race Ethnicity and Asthma Geneticsmentioning

confidence: 99%

Applying epidemiologic concepts of primary, secondary, and tertiary prevention to the elimination of racial disparities in asthma

Joseph

Williams

Ownby

et al. 2006

Journal of Allergy and Clinical Immunology

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Despite medical and scientific advances, racial and ethnic disparities persist in US asthma morbidity and mortality rates. Progress in the elimination of these disparities will involve disentangling the contribution of social constructs, such as race, socioeconomic status, and culture, from that of the physical environment and genetic susceptibility. One approach to reducing asthma disparities is through the traditional disease prevention stages of intervention. As such, primary prevention targets reductions in asthma incidence; secondary prevention is the mitigation of established disease and involves disease detection, management, and control; and tertiary prevention is the reduction of complications caused by severe disease. Once causative factors at each level of disease prevention are understood, this knowledge can be translated into clinical practice and public health policy.

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“…Discrepancy between our results and those of Barnes et al may also be due to a difference in the environmental factors of the two study populations. There are a number of studies showing that the effects of genetic variation (-159C/T) of the CD14 gene on allergic sensitization and BA risk differ greatly due to environmental factors such as mite or lipopolysacharide concentration in dust (Ober et al 2000;Simpson et al 2006;Vercelli 2003;Zambelli-Weiner et al 2005). It may be possible that C3 gene variations also show this type of geneenvironmental interaction and cause discrepant results in studies with different populations.…”

Section: Discussionmentioning

confidence: 99%

Association study of the C3 gene with adult and childhood asthma

et al. 2008

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Bronchial asthma (BA) is a multifactorial disorder, the development of which is affected by both environmental and genetic factors. The complement system plays an important role in immunological response against invading microorganisms. It has been shown that complement-C3-deficient mice have reduced inflammation of asthmatic airways. Previously, we reported the association of four single nuclear proteins (SNPs) in the exons of the C3 gene with childhood and adult BA. The C3 gene, however, is a large gene, and functional SNPs associated with susceptibility to BA have not yet been identified. We analyzed 26 SNPs in the C3 gene and its promoter region to narrow down the regions showing association with childhood and adult BA. Childhood and adult atopic BA patients and healthy child and adult controls were recruited from urban cities in Japan and genotyped. In SNP analysis, an SNP (SNP24, rs11569562) located in intron 31 of the C3 gene was associated with adult BA [corrected P (P cor ) = 0.030]. In linkage disequilibrium (LD) block 4 spanning exons 24-41, the frequency of the CCC haplotype in adult BA was significantly higher than that in adult controls (P cor = 0.038). Neither the SNP nor the haplotype showing association with adult BA demonstrated a significant association with serum total immunoglobulin E (IgE) level in BA patients and controls. Our results suggest that LD block 4 confers susceptibility to adult BA with mechanisms relevant to the effector phase of allergic inflammation.

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Evaluation of the CD14/-260 polymorphism and house dust endotoxin exposure in the Barbados Asthma Genetics Study

Cited by 140 publications

References 36 publications

Gene Encoding Duffy Antigen/Receptor for Chemokines Is Associated with Asthma and IgE in Three Populations

Gene Encoding Duffy Antigen/Receptor for Chemokines Is Associated with Asthma and IgE in Three Populations

Applying epidemiologic concepts of primary, secondary, and tertiary prevention to the elimination of racial disparities in asthma

Association study of the C3 gene with adult and childhood asthma

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