Background: Atopic dermatitis (AD) shows differential clinical presentation in older compared with younger patients. Nevertheless, changes in the AD molecular profile with age are unknown. Objective: We sought to characterize age-related changes in the AD profile. Methods: We evaluated age-specific changes in lesional and nonlesional tissues and blood from patients with moderate-tosevere AD (n 5 246) and age-matched control subjects (n 5 71) using immunohistochemistry, quantitative real-time PCR, and Singulex in a cross-sectional study. Patients were analyzed by age group (18-40, 41-60, and > _61 years). Results: Although disease severity/SCORAD scores were similar across AD age groups (mean, approximately 60 years; P 5 .873), dendritic cell infiltrates (CD1b 1 and FcεRI 1 , P < .05) decreased with age. T H 2 measures (IL5, IL13, CCL13, CCL18, and CCL26) significantly decreased with age in patients with AD, despite increasing with age in control subjects. Consistent with T H 2 axis decreases, serum IgE levels and eosinophil counts negatively correlated with age in patients with AD (r 5 20.24 and r 5 20.23, respectively; P < .05). T H 22-secreted IL22 expression levels also decreased with age uniquely in patients with AD (P < .05). Expression of T H 1-related (IFNG, IL12/23p40, STAT1, and CXCL9; P < .05 for CXCL9) and T H 17-related (IL17A and IL20; P < .05 for IL20) markers increased with age in both patients with AD and control subjects. Expression of terminal differentiation measures significantly increased in older patients with AD (loricrin [LOR] and filaggrin [FLG], P < .05), whereas expression of S100As (S100A8, P < .01) and hyperplasia markers (epidermal thickness, keratin 16, and Ki67; P < .05 for keratin 16) decreased. Serum trends in AD mimicked skin findings, with T H 2 downregulation (CCL26; r 5 20.32, P < .1) and T H 1 upregulation (IFN-g; r 5 0.48, P < .01) with age. Conclusion: The adult AD profile varies with age. Although T H 1/T H 17 skewing increases in both patients with AD and control subjects, patients with AD show unique decreases in T H 2/T H 22 polarization and normalization of epithelial abnormalities. Thus age-specific treatment approaches might be beneficial for AD.

Background: Oxidative stress associated with postprandial lipemia contributes to endothelial dysfunction, which shifts hemostasis to a more thrombogenic state. Objective: We investigated whether a high concentration of phenols in olive oil can partly reverse this phenomenon. Design: Twenty-one hypercholesterolemic volunteers received 2 breakfasts rich in olive oils with different phenolic contents (80 or 400 ppm) according to a randomized, sequential crossover design. Plasma concentrations of lipid fractions, factor VII antigen (FVIIag), activated factor VII (FVIIa), and plasminogen activator inhibitor-1 (PAI-1) activity were measured at baseline and postprandially. Results: Concentrations of FVIIa increased less (P ҃ 0.018) and plasma PAI-1 activity decreased more (P ҃ 0.021) 2 h after the high-phenol meal than after the low-phenol meal. FVIIa concentrations 120 min after intake of the olive oil with a high phenol content correlated positively with fasting plasma triacylglycerols (P ҃ 0.001), area under the curve (AUC) of triacylglycerols (P ҃ 0.001), and AUC of nonesterified fatty acids (P ҃ 0.024) and negatively with hydroxytyrosol plasma concentrations at 60 min (P ҃ 0.039) and fasting HDL-cholesterol concentrations (P ҃ 0.005). PAI-1 positively correlated with homeostasis model assessment of insulin resistance (P ҃ 0.005) and fasting triacylglycerols (P ҃ 0.025) and inversely with adiponectin (P ҃ 0.026). In a multivariate analysis, the AUCs of nonesterified fatty acids (R 2 ҃ 0.467; ␤: 0.787; SE: 0.02; P 0.001) and adiponectin (R 2 ҃ 0.232; ␤: Ҁ1.594; SE: 0.629; P 0.05) were the strongest predictors of plasma FVIIa and PAI-1, respectively.