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Association of Early Life Circulating TSLP Differs by Race among Children with Atopic Dermatitis in the Mechanisms of Progression from Atopic Dermatitis to Asthma in Children (MPAACH) Cohort

ˆThe ‰journal of allergy and clinical immunology/Journal of allergy and clinical immunology/˜The œjournal of allergy and clinical immunology(2020)

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摘要
Thymic stromal lymphopoietin (TSLP) is an epithelial cytokine strongly implicated in atopic dermatitis (AD) and asthma pathogenesis. AD and asthma have a higher prevalence in black populations. However, the interplay between TSLP, race, and pediatric AD and asthma is unknown. We aimed to determine whether circulating TSLP was associated with demographic and clinical factors in a race-specific fashion using the Mechanisms of Progression from AD to Asthma in Children (MPAACH) cohort of children with AD. We conducted overall and race-stratified analyses of the association between plasma TSLP levels and demographic and clinical outcomes among children age 0.25-2.95 years with AD in the MPAACH study. We measured plasma TSLP levels by ELISA. We detected plasma TSLP in 381 subjects (94% of available samples); 231 black, 149 non-black. Among all subjects, increased TSLP was significantly associated with age (p=0.04), weight (p=0.01), birth season (p=0.002), serum vitamin D (p=0.04), lesional FLG (p=0.05), sensitization load (p=0.0007) and sensitization profile (p=0.008). Median plasma TSLP was decreased in black (63.9 pg/ml) compared with non-black children (70.8 pg/ml, p=0.10). Among black children, increased TSLP was associated with birth season (p=0.0003), non-lesional TEWL (p=0.08), sensitization load (p=0.0008) and sensitization profile (p=0.001). In non-black children, increased TSLP was associated with age (p=0.003), weight (p=0.004), lesional S100A8 (p=0.04), no reported food allergy (p=0.04), and wheeze without a cold (p=0.04). Early life circulating TSLP associations with demographic and clinical outcomes differed by race in pediatric AD. These associations suggest key race-specific differences in AD and asthma pathogenesis.
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