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Relationship between childhood atopy and wheeze: what mediates wheezing in atopic phenotypes?
Ramesh J Kurukulaaratchy1, Sharon Matthews, S Hasan Arshad
1The David Hide Asthma & Allergy Research Centre, St Mary's Hospital, Newport, Isle of Wight, England.
Insights
Childhood wheeze is strongly linked to chronic atopy, influenced by genetics and environmental factors. Other atopic phenotypes show varied wheeze patterns, with some protected by breastfeeding.
Area of Science:
- Pediatric Allergy and Immunology
- Respiratory Medicine
- Epidemiology
Background:
- The relationship between childhood wheeze and atopy (allergic sensitization) is not fully understood.
- Identifying distinct atopic phenotypes is crucial for understanding wheeze development.
Purpose of the Study:
- To characterize childhood wheeze patterns across different atopic phenotypes.
- To identify risk factors for wheeze onset in a longitudinal birth cohort.
Main Methods:
- Longitudinal birth cohort study (N=1,456) recruited in 1989.
- Children assessed at birth and ages 1, 2, 4, and 10.
- Skin prick testing at ages 4 and 10 defined atopic phenotypes; logistic regression identified risk factors.
Main Results:
- Wheeze prevalence varied by atopic phenotype: 37% (never atopic), 38% (early), 65% (chronic), 52% (delayed).
- Chronic childhood atopy showed significant wheezing morbidity and bronchial hyperresponsiveness, linked to male sex, early eczema, family history, and early tobacco exposure.
- Exclusive breastfeeding protected against early childhood atopic wheeze; maternal asthma, urticaria history, and dog ownership increased delayed atopic wheeze.
Conclusions:
- Chronic childhood atopy is associated with the most severe forms of childhood wheezing.
- Wheeze onset in chronic atopy involves genetic factors, allergens, and environmental triggers.
- In non-atopic children, environmental factors and genetic predisposition are key for wheezing.
Background:
The nature of the relationship between childhood wheeze and atopy remains uncertain.
Objective:
To characterize childhood wheeze among atopic phenotypes in a longitudinal birth cohort study.
Methods:
A whole population birth cohort (N = 1,456) was recruited in 1989. Children were seen at birth and at 1, 2, 4, and 10 years of age to obtain information on asthma and allergic disease development and relevant risk factors for these states. Skin prick testing at ages 4 (n = 980) and 10 (n = 1,036) years was used to define atopic phenotypes. Wheezing in these states was characterized, and logistic regression was used to identify independent risk factors for wheeze onset in different atopic phenotypes.
Results:
Wheeze ever occurred in 37% of never atopics, 38% of early childhood atopics, 65% of chronic childhood atopics, and 52% of delayed childhood atopics. Chronic childhood atopics had significant wheezing morbidity and bronchial hyperresponsiveness. Their wheezing was associated with male sex, early eczema, family history of eczema, and early tobacco exposure. Never atopic wheeze was related to maternal asthma, parental smoking, and respiratory tract infections. Exclusive breastfeeding protected against early childhood atopic wheeze. Maternal asthma, family history of urticaria, and dog ownership increased delayed childhood atopic wheeze.
Conclusions:
In many respects, chronic childhood atopy is the atopic phenotype associated with the most significant forms of childhood wheezing. In such children, heritable drive, allergens, and synergy with other environmental triggers seem to be crucial determinants of wheeze onset. Where such sensitization is absent, numerous environmental factors plus genetic predisposition may assume importance for wheezing.
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