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. 2024 Dec;35(12):e70014.
doi: 10.1111/pai.70014.

Molecular allergen sensitization drives phenotypes of severe asthma in children: Evidence from a megacity cohort (SAMP)

Mélisande Bourgoin-Heck  1   2   3 , Victoria Wolff-Goldnadel  1 , Yannick Chantran  2   4 , Sarah Saf  1 , Tamazoust Guiddir  5 , Flore Amat  6   7 , Fanny Rancière  2   8 , Isabelle Momas  2   8 , Stéphanie Wanin  1   2 , Thierry Rose  3 , Philippe Saint-Pierre  9 , Jocelyne Just  2   10
Affiliations

Molecular allergen sensitization drives phenotypes of severe asthma in children: Evidence from a megacity cohort (SAMP)

Mélisande Bourgoin-Heck et al. Pediatr Allergy Immunol. 2024 Dec.

Abstract

Background: Several major sensitization profiles have been described in children with asthma, but it remains unclear how these profiles relate to asthma phenotypes. The aim of this study was to determine allergenic sensitization profiles in a megacity cohort (SAMP).

Methods: This was a cross-sectional analysis performed from 2011 to 2015 including preschool and school-age children with severe and moderate asthma from the SAMP cohort. We performed ALEX multiplex array and carried out cluster analysis.

Results: Data from 367 children were analyzed: 224 of preschool age and 143 of school age, respectively 84 (38%) and 114 (80%) presented at least one allergic sensitization. At preschool age, three clusters were identified: Cluster 1, Few sensitizations to inhaled allergen molecular families and non-type 2 (T2) inflammation (n = 61); Cluster 2, Predominant sensitization to HDM molecular families (n = 16); Cluster 3, Severe asthma with multiple sensitizations to inhaled and food allergen molecular families (n = 7). At school age, five clusters were identified: Cluster 1, Few sensitizations to inhaled allergen molecular families and non-T2 inflammation (n = 43); Cluster 2, Predominant sensitization to HDM molecular families (n = 31); Cluster 3, Predominant sensitization to PR-10 protein family (n = 25); Cluster 4, Severe asthma with predominant sensitization to tropomyosin family (n = 11); Cluster 5, Severe asthma with multiple sensitizations to inhaled and food allergen molecular families (n = 4).

Conclusion: These results underline the heterogeneity of sensitization profiles in severe allergic childhood asthma. The most severe asthma phenotypes were associated with multiple sensitizations to both inhaled and food allergen molecular families as expected, and to the tropomyosin molecular family, a novel finding.

Keywords: ALEX multiplex array; asthma phenotype; children; severe asthma; type 2 inflammation.

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Conflict of interest statement

Melisande Bourgoin‐Heck declares consultancy for Biocryst, CSL‐Behring, Takeda and ALK; Flore Amat declares consultancy for Stallergenes‐Greer and ALK, speaker's fee from Stallergene‐Greer, DBV and Sanofi; Stéphanie Wanin received speaker/consulting fees from Aimmune Therapeutics, ALK, AstraZeneca, GSK, Novartis, Sanofi, Regeneron Pharmaceuticals Inc.; Jocelyne Just received research grants from Novartis and Astra Zeneca, and received fees for lectures and consulting activities from ALK‐Abello, Astra Zeneca, GSK, Sanofi, Stallergenes; Victoria Wolff‐Goldnadel, Yannick Chantran, Sarah Saf, Fanny Ranciere, Isabelle Momas, Philippe Saint‐Pierre, Tamazoust Guiddir and Tierry Rose declare no conflict of interest.

Figures

FIGURE 1
FIGURE 1
Correlation network of a set of component‐specific IgE at school age. The nodes representing sIgE are colored according to the hierarchical clustering analysis (Figure S1). A Pearson's correlation coefficient greater than .5 is represented by an edge between two nodes. Edge width represents the strength of correlation between pairs of sIgE components. sIgE, specific immunoglobulin E.
FIGURE 2
FIGURE 2
Representation of the five school‐age clusters according to FEV1, hospitalizations for severe asthma exacerbation, and total IgE. FEV1 is expressed as percentage of predicted values, and hospitalizations as mean number during last year. Circled areas represent mean total IgE in kUI/L.
See this image and copyright information in PMC

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