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Proteomic characterization of atopic dermatitis blood from infancy to adulthood
Ester Del Duca1, Yael Renert-Yuval2, Ana B Pavel3
1Department of Dermatology and Laboratory of Inflammatory Skin Diseases, Icahn School of Medicine at Mount Sinai, New York; Department of Dermatology, University of Magna Graecia, Catanzaro, Italy.
Insights
Atopic dermatitis (AD) shows distinct age-specific immune system changes. Infants exhibit early inflammation, while adults develop unique cardiovascular and diabetes-related protein signatures, highlighting the need for age-tailored treatments.
Area of Science:
- Immunology
- Proteomics
- Dermatology
Background:
- Atopic dermatitis (AD) involves systemic biomarker dysregulation that varies with age.
- The specific proteomic changes associated with age-based differences in AD are not well understood.
Purpose of the Study:
- To comprehensively profile blood proteins in patients with atopic dermatitis across various age groups.
- To compare these proteomic profiles with age-matched healthy controls.
Main Methods:
- Utilized the Olink high-throughput proteomic platform to analyze serum proteins.
- Examined 375 proteins in 20 infants, 39 children, 21 adolescents, and 20 adults with moderate-to-severe AD.
- Included 83 age-appropriate control subjects for comparison.
Main Results:
- Identified distinct proteomic signatures for each age group with AD.
- Observed age-dependent shifts in Th2 and Th1 immune responses.
- Infants with AD showed early signs of systemic inflammation, including innate immunity and T-cell activation markers.
- Adults with AD exhibited unique upregulation of proteins linked to cardiovascular health and diabetes.
Conclusions:
- Systemic immune signatures in AD are age-specific, extending beyond general Th2 activation.
- These findings support the development of precision medicine strategies tailored to individual age-related AD profiles.
Background:
Patients with atopic dermatitis (AD) have systemic biomarker dysregulation that differs by age group; however, the proteomic characteristics of these age-based changes are unknown.
Objective:
To profile blood proteins of patients with AD across different age groups versus age-appropriate controls.
Methods:
Using the Olink high-throughput proteomic platform, we profiled 375 serum proteins of 20 infants (age, 0-5 years), 39 children (age, 6-11 years), 21 adolescents (age, 12-17 years), and 20 adults (age, ≥18 years) with moderate-to-severe AD and 83 age-appropriate controls.
Results:
Each group presented a distinct systemic proteomic signature. Th2-related proteins were increased in infant AD and further intensified with age through adolescence and adulthood (interleukin 4/CCL13/CCL17). In contrast, Th1 axis down-regulation was detected in infants with AD and gradually reversed to increased Th1 products (interferon γ/CXCL9/CXCL10/CCL2) in patients with AD from childhood to adulthood. Despite their short disease duration, infants already had evidence of systemic inflammation, with significant upregulation of innate immunity (interleukin 17C/ interleukin-1RN), T-cell activation/migration (CCL19), Th2 (CCL13/CCL17), and Th17 (PI3) proteins. Adults with AD present unique upregulation of cardiovascular proteins related to coagulation and diabetes.
Limitations:
Cross-sectional observational study with a single time point.
Conclusion:
Systemic immune signatures of AD are age-specific beyond the shared Th2 immune activation. These data advocate for precision medicine approaches based on age-specific AD profiles.
