Cited by 118Asthma and respiratory diseasesHealth disparities and outcomesEnvironmental Justice and Health Disparities

Genome-wide transcriptional profiling linked to social class in asthma

Open access
Chen, E, Miller, G E, Walker, H A, Arevalo, J M, Sung, C Y, Cole, S W·2008·Thorax

Abstract

OBJECTIVES: Low socioeconomic status (SES) is one of the most robust social factors associated with disease morbidity, including more severe asthma in childhood. However, our understanding of the biological processes that explain this link is limited. This study tested whether the social environment could get "under the skin" to alter genomic activity in children with asthma. DESIGN AND PARTICIPANTS: Two group design of children with physician diagnosed asthma who came from low or high SES families. OUTCOMES: Genome-wide transcriptional profiles from T lymphocytes of children with asthma. RESULTS: Children with asthma from a low SES background showed overexpression of genes regulating inflammatory processes, including those involved in chemokine activity, stress responses and wound responses, compared with children with asthma from a high SES background. Bioinformatic analysis suggested that decreased activity of cyclic AMP response element binding protein and nuclear factor Y and increased nuclear factor kappaB transcriptional signalling mediated these effects. These pathways are known to regulate catecholamine and inflammatory signalling in immune cells. CONCLUSIONS: This study provides the first evidence in a sample of paediatric patients diagnosed with asthma that the larger social environment can affect processes at the genomic level. Specifically, gene transcription control pathways that regulate inflammation and catecholamine signalling were found to vary by SES in children with asthma. Because these pathways are the primary targets of many asthma medications, these findings suggest that the larger social environment may alter molecular mechanisms that have implications for the efficacy of asthma therapeutics.

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Crossref · 10.1136/thx.2007.095091

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  • Several studies have demonstrated that hundreds of genes are differentially expressed as a function of several types of social adversity, including social isolation, low social status, or chronic interpersonal stress.

    “several studies have demonstrated that literally hundreds of genes are differentially expressed as a function of several types of social adversity, including being socially isolated or low in social status, or experiencing high levels of chronic interpersonal stress”

    From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Chen et al., 2009

    The Results (Differential gene expression; page unavailable) report gene-expression differences by socioeconomic status in children with asthma, supporting the low-status example. But the study found 56 distinct genes, not hundreds, and our copy does not establish comparable findings for social isolation or chronic interpersonal stress. (LLM, conf=0.90)

    Experimental — accuracy not yet measured
  • A small number of studies have found genomewide transcriptional shifts in persons with asthma, ovarian cancer, breast cancer, and posttraumatic stress disorder.

    “a small number of studies have found genomewide transcriptional shifts in persons with asthma, ovarian cancer, breast cancer, and posttraumatic stress disorder”

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Authors
Chen, E., Miller, G. E., Walker, H. A., Arevalo, J. M., Sung, C. Y., & Cole, S. W.
Affiliations
  • University of British Columbia (CA)
  • University of California, Los Angeles (US)
Corresponding author
Chen, E
Venue
Thorax
Publisher
BMJ
Published
2008-10-03
Volume
64
Issue
1
Pages
38-43
ISSN
0040-6376 (ISSN-L)
OpenAlex
W2169048270
Cited by
118
References
1
Citations by year
2025: 1 · 2024: 4 · 2023: 3 · 2022: 8 · 2021: 7 · 2020: 4 · 2019: 3 · 2018: 10 · 2017: 8 · 2016: 9 · 2015: 5 · 2014: 11 · 2013: 10 · 2012: 14
FWCI
4.75
Type
journal article
Language
en
Open access
Locations
  • Thorax (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • HighWire Press Open Archive (submittedVersion)
Funders
  • National Institutes of Health
  • Canadian Institutes of Health Research
  • National Heart, Lung, and Blood Institute (HL073975, R01HL073975)
  • National Cancer Institute (R01CA116778)
Topics
  • Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
  • Social Sciences › Health › Health disparities and outcomes
  • Social Sciences › Sociology and Political Science › Environmental Justice and Health Disparities
Keywords
childhood asthma, socioeconomic status, social class, gene expression profiling, T cells, inflammation, chemokines, stress response, wounding response, cyclic AMP response element binding protein, nuclear factor-kappaB, asthma treatment
MeSH terms
Asthma, Child, Female, Humans, Male, Prognosis, Social Class, Transcription, Genetic, Genome, Human, Gene Expression Profiling

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