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Published on: April 8, 2016
Atopic dermatitis phenotype affects expression of atopic diseases despite similar mononuclear cell cytokine response
Mohamed H Taki1, Kristine E Lee2, Ronald Gangnon2
1Department of Pediatrics, University of Wisconsin School of Medicine and Public Health, Madison, Wis; Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wis.
Insights
Atopic dermatitis (AD) phenotype influences the development of other allergic diseases. However, immune dysregulation in the blood does not appear to drive this atopic march, suggesting localized immune responses.
Area of Science:
- Pediatric Allergy and Immunology
- Immunology
- Dermatology
Background:
- The atopic march describes the progression of allergic diseases in childhood, often starting with atopic dermatitis (AD).
- Understanding the factors influencing the atopic march is crucial for early intervention and management of childhood allergic diseases.
Purpose of the Study:
- To investigate if atopic dermatitis (AD) phenotype modifies the risk of developing subsequent atopic diseases.
- To explore whether underlying cytokine signaling dysregulation contributes to these observed differences.
Main Methods:
- Prospective follow-up of 285 children from the Childhood Origins of Asthma (COAST) birth cohort from birth to 18 years.
- Assessment of atopic dermatitis (AD), food allergy, allergic rhinitis, and asthma rates.
- Analysis of associations between AD phenotype and allergic outcomes, including sensitization and lung function, alongside peripheral blood mononuclear cell cytokine responses.
Main Results:
- Early-onset atopic dermatitis (AD) at year 1 was linked to a higher risk of food allergy.
- Persistent and late-onset AD were associated with increased risks of asthma, allergic rhinitis, elevated IgE, and exhaled nitric oxide.
- No consistent differences in peripheral blood cytokine responses were found among different AD phenotypes.
Conclusions:
- Atopic dermatitis (AD) phenotype is associated with distinct patterns of other atopic disease development.
- Peripheral blood cytokine dysregulation does not appear to be the primary mechanism driving the atopic march.
- Immune dysregulation in the atopic march may occur at mucosal surfaces or secondary lymphoid organs.
Background:
The atopic march refers to the coexpression and progression of atopic diseases in childhood, often beginning with atopic dermatitis (AD), although children may not progress through each atopic disease.
Objective:
We hypothesized that future atopic disease expression is modified by AD phenotype and that these differences result from underlying dysregulation of cytokine signaling.
Methods:
Children (n = 285) were enrolled into the Childhood Origins of Asthma (COAST) birth cohort and followed prospectively. Rates of AD, food allergy, allergic rhinitis, and asthma were assessed longitudinally from birth to 18 years of age. Associations between AD phenotype and food allergy, allergic rhinitis, asthma, allergic sensitization, exhaled nitric oxide, and lung function were determined. Peripheral blood mononuclear cell responses (IL-5, IL-10, IL-13, IFN-γ) to dust mite, phytohemagglutinin, Staphylococcus aureus Cowan I, and tetanus toxoid were compared among AD phenotypes.
Results:
AD at year 1 was associated with an increased risk of food allergy (P = .004). Both persistent and late-onset AD were associated with an increased risk of asthma (P < .001), rhinitis (P < .001), elevated total IgE (P < .001), percentage of aeroallergens with detectable IgE (P < .001), and elevated exhaled nitric oxide (P = .002). Longitudinal analyses did not reveal consistent differences in peripheral blood mononuclear cell responses among dermatitis phenotypes.
Conclusion:
AD phenotype is associated with differential expression of other atopic diseases. Our findings suggest that peripheral blood cytokine dysregulation is not a mechanism underlying this process, and immune dysregulation may be mediated at mucosal surfaces or in secondary lymphoid organs.
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