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Divergent transcriptional profiles in pediatric asthma patients of low and high socioeconomic status
Author(s) -
Miller Gregory E.,
Chen Edith,
Shalowitz Madeleine U.,
Story Rachel E.,
Leigh Adam K. K.,
Ham Paula,
Arevalo Jesusa M. G.,
Cole Steve W.
Publication year - 2018
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/ppul.23983
Subject(s) - medicine , socioeconomic status , asthma , immunology , cytokine , disease , t helper cell , tumor necrosis factor alpha , environmental health , t cell , immune system , population
Aim There are marked socioeconomic disparities in pediatric asthma control, but the molecular origins of these disparities are not well understood. To fill this gap, we performed genome‐wide expression profiling of monocytes and T‐helper cells from pediatric asthma patients of lower and higher socioeconomic status (SES). Method Ninety‐nine children with asthma participated in a cross‐sectional assessment. Out of which 87% were atopic, and most had disease of mild (54%) or moderate (29%) severity. Children were from lower‐SES ( n = 49; household income <$50 000) or higher‐SES ( n = 50; household income >$140 000) families. Peripheral blood monocytes and T‐helper cells were isolated for genome‐wide expression profiling of mRNA. Results Lower‐SES children had worse asthma quality of life relative to higher‐SES children, by both their own and their parents’ reports. Although the groups had similar disease severity and potential confounds were controlled, their transcriptional profiles differed notably. The monocytes of lower‐SES children showed transcriptional indications of up‐regulated anti‐microbial and pro‐inflammatory activity. The T‐helper cells of lower‐SES children also had comparatively reduced expression of genes encoding γ‐interferon and tumor necrosis factor‐α, cytokines that orchestrate Type 1 responses. They also showed up‐regulated activity of transcription factors that polarize cells towards Type 2 responses and promote Th17 cell maturation. Conclusion Collectively, these patterns implicate pro‐inflammatory monocytes and Type 2 cytokine activity as mechanisms contributing to worse asthma control among lower‐SES children.