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Published on: September 27, 2017
Early-onset pediatric atopic dermatitis is characterized by TH2/TH17/TH22-centered inflammation and lipid alterations
Patrick M Brunner1, Ariel Israel2, Ning Zhang3
1Laboratory for Investigative Dermatology, Rockefeller University, New York, NY.
Insights
Pediatric atopic dermatitis (AD) shows distinct immune and barrier defects compared to adult AD. Early-onset AD in infants lacks the epidermal changes seen in adults, suggesting chronic inflammation drives these differences.
Area of Science:
- Dermatology
- Immunology
- Molecular Biology
Background:
- Atopic dermatitis (AD) frequently begins in early childhood, yet detailed skin profiling of early-onset pediatric AD is limited.
- This knowledge gap hinders the development of targeted therapies for children with significant unmet needs.
Purpose of the Study:
- To globally profile the skin of infants with early-onset AD.
- To compare these findings with adult AD and healthy control skin.
Main Methods:
- Microarray, RT-PCR, and fluorescence microscopy were used.
- Studies were conducted on infants and young children (<5 years) with early-onset AD (<6 months disease duration).
- Comparisons were made with age-matched controls and adults with longstanding AD.
Main Results:
- Pediatric and adult AD show distinct transcriptomic profiles in lesional and nonlesional skin.
- Both groups exhibit TH2-centered inflammation, but pediatric AD also shows TH17/TH22 skewing without the TH1 upregulation seen in adults.
- Pediatric AD has relatively normal epidermal differentiation products, unlike adults, but shares lipid barrier and tight junction defects. Specific lipid mediator genes were preferentially downregulated in pediatric AD.
Conclusions:
- Shared defects in lipid metabolism and tight junctions exist between pediatric and adult AD.
- Epidermal differentiation complex defects are unique to adult AD, likely due to chronic immune dysregulation.
- These findings highlight key differences in disease mechanisms between early-onset and longstanding atopic dermatitis.
Background:
Although atopic dermatitis (AD) often starts in early childhood, detailed tissue profiling of early-onset AD in children is lacking, hindering therapeutic development for this patient population with a particularly high unmet need for better treatments.
Objective:
We sought to globally profile the skin of infants with AD compared with that of adults with AD and healthy control subjects.
Methods:
We performed microarray, RT-PCR, and fluorescence microscopy studies in infants and young children (<5 years old) with early-onset AD (<6 months disease duration) compared with age-matched control subjects and adults with longstanding AD.
Results:
Transcriptomic analyses revealed profound differences between pediatric patients with early-onset versus adult patients with longstanding AD in not only lesional but also nonlesional tissues. Although both patient populations harbored TH2-centered inflammation, pediatric AD also showed significant TH17/TH22 skewing but lacked the TH1 upregulation that characterizes adult AD. Pediatric AD exhibited relatively normal expression of epidermal differentiation and cornification products, which is downregulated in adults with AD. Defects in the lipid barrier (eg, ELOVL fatty acid elongase 3 [ELOVL3] and diacylglycerol o-acyltransferase 2 [DGAT2]) and tight junction regulation (eg, claudins 8 and 23) were evident in both groups. However, some lipid-associated mediators (eg, fatty acyl-CoA reductase 2 and fatty acid 2-hydroxylase) showed preferential downregulation in pediatric AD, and lipid barrier genes (FA2H and DGAT2) showed inverse correlations with transepidermal water loss, a functional measure of the epidermal barrier.
Conclusions:
Skin samples from children and adult patients with AD share lipid metabolism and tight junction alterations, but epidermal differentiation complex defects are only present in adult AD, potentially resulting from chronic immune aberration that is not yet present in early-onset disease.
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