Literature DB >> 29528197

Divergent transcriptional profiles in pediatric asthma patients of low and high socioeconomic status.

Gregory E Miller1, Edith Chen1, Madeleine U Shalowitz2, Rachel E Story2, Adam K K Leigh1, Paula Ham1, Jesusa M G Arevalo3, Steve W Cole3.   

Abstract

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.
© 2018 Wiley Periodicals, Inc.

Entities:  

Keywords:  asthma; cytokines; health disparities; pediatrics

Mesh:

Substances:

Year:  2018        PMID: 29528197      PMCID: PMC5992048          DOI: 10.1002/ppul.23983

Source DB:  PubMed          Journal:  Pediatr Pulmonol        ISSN: 1099-0496


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