Integrative genomic analysis identifies a role for intercellular adhesion molecule 1 in childhood asthma

Klaassen, Ester M.M.; Kant, Kim D. G. van de; Jöbsis, Quirijn; Penders, John; Schooten, Frederik J. van; Quaak, Marieke; Hartog, G.J.M. den; Koppelman, Gerard H.; Schayck, C.P. van; Eys, Guillaume van; Dompeling, Edward

doi:10.1111/pai.12187

Cited by 19 publications

(17 citation statements)

References 29 publications

(38 reference statements)

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“…The allele frequencies of rs5491 and rs5498 in our data were similar to the Chinese data in the HapMap project and the results of another two Chinese studies [31,32]. Both of the studied ICAM1 SNPs were functional SNPs, so they could influence the encoded enzyme [23,24,33]. …”

Section: Discussionsupporting

confidence: 86%

“…However, Li et al indicated that the risk for asthma was higher in rs5491 T allele carriers [22]. The ICAM1 rs5498 A allele had been reported to be positively associated with childhood asthma in African-Americans [22], Germans [23], and the Dutch [24]. The ICAM1 haplotype of rs5493 (G241S) and rs5498 [22], and another haplotype of rs5498 and rs885743 (in the 3’-untranslated region) [23] were reported to be associated with the risk for childhood asthma.…”

Section: Discussionmentioning

confidence: 99%

“…ICAM1 is the most important receptor of human rhinovirus infection [18], and some studies have found that asthma can also be induced by rhinovirus infection [19,20,21]. Many single-nucleotide polymorphisms (SNPs) of ICAM1 have been reported, and some of these SNPs, such as rs5491 (K56M) and rs5498 (K469E), are now known to be associated with asthma [22,23,24]. However, the association between ICAM1 SNPs/haplotypes and childhood asthma has not yet been studied previously in a Chinese population.…”

Section: Introductionmentioning

confidence: 99%

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Interaction of Intercellular Adhesion Molecule 1 (ICAM1) Polymorphisms and Environmental Tobacco Smoke on Childhood Asthma

Lin

Tai

2014

IJERPH

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Asthma is a chronic disease that is particularly common in children. The association between polymorphisms of the gene encoding intercellular adhesion molecule 1 (ICAM1) and gene-environment interactions with childhood asthma has not been fully investigated. A cross-sectional study was undertaken to investigate these associations among children in Taiwan. The effects of two functional single-nucleotide polymorphisms (SNPs) of ICAM1, rs5491 (K56M) and rs5498 (K469E), and exposure to environmental tobacco smoke (ETS) were studied. Two hundred and eighteen asthmatic and 877 nonasthmatic children were recruited from elementary schools. It was found that the genetic effect of each SNP was modified by the other SNP and by exposure to ETS. The risk of asthma was higher for children carrying the rs5491 AT or TT genotypes and the rs5498 GG genotype (odds ratio = 1.68, 95% confidence interval 1.09–2.59) than for those with the rs5491 AA and rs5498 AA or AG genotypes (the reference group). The risk for the other two combinations of genotypes did not differ significantly from that of the reference group (p of interaction = 0.0063). The two studied ICAM1 SNPs were associated with childhood asthma among children exposed to ETS, but not among those without ETS exposure (p of interaction = 0.05 and 0.01 for rs5491 and rs5498, respectively). Both ICAM1 and ETS, and interactions between these two factors are likely to be involved in the development of asthma in childhood.

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Section: Discussionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Interaction of Intercellular Adhesion Molecule 1 (ICAM1) Polymorphisms and Environmental Tobacco Smoke on Childhood Asthma

Lin

Tai

2014

IJERPH

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“…This is problematic because the majority of genomic studies do not implicitly model sex interaction effects [10, 34, 35]. Further, many two-step genome-wide approaches to test interaction assume main (marginal) effects [36, 37].…”

Section: Discussionmentioning

confidence: 99%

Genomic architecture of asthma differs by sex

et al. 2015

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Asthma comprised of highly heterogeneous subphenotypes resulting from complex interplay between genetic and environmental stimuli. While much focus has been placed on extrinsic environmental stimuli, intrinsic environment such as sex can interact with genes to influence asthma risk. However, few studies have examined sex-specific genetic effects. The overall objective of this study was to evaluate if sex-based differences exist in genomic associations with asthma. We tested 411 asthmatics and 297 controls for presence of interactions and sex-stratified effects in 51 genes using both SNP and gene expression data. Logistic regression was used to test for association. Over half (55%) of the genetic variants identified in sex-specific analyses were not identified in the sex-combined analysis. Further, sex-stratified genetic analyses identified associations with significantly higher median effect sizes than sex-combined analysis for girls (p-value =6.5E-15) and for boys (p-value =1.0E-7). When gene expression data was analyzed to identify genes that were differentially expressed in asthma versus non-asthma, nearly one third (31%) of the probes identified in the sex-specific analyses were not identified in the sex-combined analysis. Both genetic and gene expression data suggest that the biologic underpinnings for asthma may differ by sex. Failure to recognize sex interactions in asthma greatly decreases the ability to detect significant genomic variation and may result in significant misrepresentation of genes and pathways important in asthma in different environments.

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“…For this purpose, noninvasive sampling in preschool age is particularly important, using, for example, exhaled breath condensate (EBC) to detect asthma development-associated biomarkers of the infiltration type (Table 1; section infiltrate-derived biomarkers), such as IL-4, IL-8, IL-10, IL-13 and sICAM1 (56). CCL-5 significantly correlates with both reduction in FEV1 and increase in airway resistance, while increased levels of TNF-a and TGF-b significantly correlate with nonspecific bronchial hyperresponsiveness.…”

Section: Disease Progression In Childrenmentioning

confidence: 99%

Current and future biomarkers in allergic asthma

Zissler

Bieren

Jakwerth

et al. 2016

Allergy

106

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Diagnosis early in life, sensitization, asthma endotypes, monitoring of disease and treatment progression are key motivations for the exploration of biomarkers for allergic rhinitis and allergic asthma. The number of genes related to allergic rhinitis and allergic asthma increases steadily; however, prognostic genes have not yet entered clinical application. We hypothesize that the combination of multiple genes may generate biomarkers with prognostic potential. The current review attempts to group more than 161 different potential biomarkers involved in respiratory inflammation to pave the way for future classifiers. The potential biomarkers are categorized into either epithelial or infiltrate-derived or mixed origin, epithelial biomarkers. Furthermore, surface markers were grouped into cell-typespecific categories. The current literature provides multiple biomarkers for potential asthma endotypes that are related to T-cell phenotypes such as Th1, Th2, Th9, Th17, Th22 and Tregs and their lead cytokines. Eosinophilic and neutrophilic asthma endotypes are also classified by epithelium-derived CCL-26 and osteopontin, respectively. There are currently about 20 epithelium-derived biomarkers exclusively derived from epithelium, which are likely to innovate biomarker panels as they are easy to sample. This article systematically reviews and categorizes genes and collects current evidence that may promote these biomarkers to become part of allergic rhinitis or allergic asthma classifiers with high prognostic value.

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Integrative genomic analysis identifies a role for intercellular adhesion molecule 1 in childhood asthma

Abstract: In this unique prospective study, we demonstrated that ICAM1 is associated with asthma development on DNA, mRNA, and protein level. Thus, ICAM1 is likely to be involved in the development of childhood asthma.

Cited by 19 publications

References 29 publications

Interaction of Intercellular Adhesion Molecule 1 (ICAM1) Polymorphisms and Environmental Tobacco Smoke on Childhood Asthma

Interaction of Intercellular Adhesion Molecule 1 (ICAM1) Polymorphisms and Environmental Tobacco Smoke on Childhood Asthma

Genomic architecture of asthma differs by sex

Current and future biomarkers in allergic asthma

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