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Identification of two early life eczema and non‐eczema phenotypes with high risk for asthma development

机译：鉴别哮喘发育高风险的早期生命湿疹和非湿疹表型

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Abstract Background The “atopic march” has been considered a linear progression starting with eczema and culminating with development of asthma. Not all asthma cases, however, are preceded by eczema, and not all children with eczema go on to develop asthma. Objective The aim of this study was to explore the impact of allergic sensitization patterns on the association between early eczema and later childhood asthma. Given the numerous reported associations of the ciliary gene KIF3A with the atopic march, we also examined the impact of KIF3A risk allele rs12186803 on our analyses. Methods We studied 505 participants in the Cincinnati Childhood Allergy and Air Pollution Study (CCAAPS), a prospective birth cohort, with longitudinal eczema and asthma outcomes as well as prospective data regarding timing of sensitization to foods and aeroallergens. KIF3A genotypes were available on all children. Results Two high‐risk groups were identified: one with and one without early eczema. The high‐risk group with early eczema was more likely to be sensitized to food allergens, while the group without early eczema was more likely to be polysensitized to aeroallergens. The KIF3A rs12186803 risk allele interacted with food sensitization to increase asthma risk in children with eczema ( P ?=?0.02). In children without eczema, asthma was associated with the interaction between rs12186803 and aeroallergen sensitization ( P ?=?0.007). Conclusions & Clinical Relevance KIF3A interacted differentially with sensitization pattern to increase the risk of asthma in two high‐risk groups of children with and without early eczema. Given the reported role of KIF3A in epithelial cell functioning, the results add evidence to the hypothesis that an impaired epithelial barrier is a key aspect in the development of allergic disease.
机译：摘要背景“Atopic 3月”被认为是从湿疹开始的线性进展，并与哮喘的发展最终。然而，并非所有哮喘案例都在湿疹之前，而不是湿疹的所有儿童都继续发展哮喘。目的本研究的目的是探讨过敏性敏感模式对早期湿疹和后期儿童哮喘之间的关联的影响。鉴于综合基因KIF3A与Atopic 3月份的许多报告的关联，我们还研究了KIF3A风险等位基因RS12186803对我们分析的影响。方法研究辛辛那提儿童过敏和空气污染研究（CCAAPS），前瞻性出生队列的505名参与者，纵向湿疹和哮喘成果以及关于对食品和航空静止的致敏时机的前瞻性数据。所有儿童都有KIF3A基因型。结果鉴定了两组高风险群体：一个没有早期湿疹的一个高风险群体。早期湿疹的高风险群更有可能对食物过敏原感到敏感，而没有早期湿疹的小组更有可能对Aeroallergens提供多敏化。 KIF3A RS12186803风险等位基因与食物致敏相互作用，以增加湿疹儿童的哮喘风险（P？= 0.02）。在没有湿疹的儿童中，哮喘与RS12186803之间的相互作用与Aeroallergen敏化（P？= 0.007）相关联。结论＆amp;临床相关性KIF3A与敏感模式差异相互作用，以提高患有早期湿疹的两个高风险儿童哮喘的风险。鉴于KIF3A在上皮细胞功能中的作用，结果为假设增加了证据，即障碍的上皮屏障是过敏性疾病发展的关键方面。

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