Bourgoin-Heck Mélisande, Wolff-Goldnadel Victoria, Chantran Yannick, Saf Sarah, Guiddir Tamazoust, Amat Flore, Rancière Fanny, Momas Isabelle, Wanin Stéphanie, Rose Thierry, Saint-Pierre Philippe, Just Jocelyne
Allergology Department, Hospital A. Trousseau, Sorbonne Université AP-HP, Paris, France.
CRESS, Inserm, INRAE, HERA Team, Université Paris Cité, Paris, France.
Pediatr Allergy Immunol. 2024 Dec;35(12):e70014. doi: 10.1111/pai.70014.
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).
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.
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).
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.
已有研究描述了哮喘儿童的几种主要致敏模式，但这些模式与哮喘表型之间的关系仍不明确。本研究的目的是确定一个大城市队列（SAMP）中的变应原致敏模式。
这是一项于2011年至2015年进行的横断面分析，纳入了SAMP队列中患有重度和中度哮喘的学龄前及学龄儿童。我们进行了ALEX多重检测并开展了聚类分析。
分析了367名儿童的数据：其中224名学龄前儿童和143名学龄儿童，分别有84名（38%）和114名（80%）至少有一种过敏致敏。在学龄前儿童中，确定了三个聚类：聚类1，对吸入性变应原分子家族致敏较少且无2型（T2）炎症（n = 61）；聚类2，主要对屋尘螨分子家族致敏（n = 16）；聚类3，对吸入性和食物变应原分子家族多重致敏的重度哮喘（n = 7）。在学龄儿童中，确定了五个聚类：聚类1，对吸入性变应原分子家族致敏较少且无T2炎症（n = 43）；聚类2，主要对屋尘螨分子家族致敏（n = 31）；聚类3，主要对PR-10蛋白家族致敏（n = 25）；聚类4，主要对原肌球蛋白家族致敏的重度哮喘（n = 11）；聚类5，对吸入性和食物变应原分子家族多重致敏的重度哮喘（n = 4）。
这些结果强调了重度过敏性儿童哮喘致敏模式的异质性。正如预期的那样，最严重的哮喘表型与对吸入性和食物变应原分子家族的多重致敏有关，并与原肌球蛋白分子家族有关，这是一个新发现。
