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Peanut allergy: effect of environmental peanut exposure in children with filaggrin loss-of-function mutations
Helen A Brough1, Angela Simpson2, Kerry Makinson1
1Department of Pediatric Allergy, Division of Asthma, Allergy and Lung Biology, King's College London and Guy's and St. Thomas' NHS Foundation Trust, London, United Kingdom.
Insights
Children with filaggrin (FLG) mutations have a higher risk of peanut allergy from early-life environmental peanut exposure. Impaired skin barrier function is key to developing peanut allergy through transcutaneous sensitization.
Area of Science:
- Dermatology
- Allergology
- Genetics
Background:
- Filaggrin (FLG) mutations impair skin barrier function, increasing peanut allergy risk.
- Household peanut consumption correlates with peanut allergen levels in dust.
Purpose of the Study:
- To investigate if environmental peanut exposure increases peanut allergy risk.
- To determine if FLG mutations modify this risk.
Main Methods:
- Assessed peanut antigen in household dust for a birth cohort.
- Measured peanut sensitization and allergy at ages 8 and 11.
- Genotyped for 6 FLG mutations.
Main Results:
- Significant interaction between FLG mutations and peanut dust levels on sensitization and allergy.
- Increased odds of sensitization (>6-fold) and allergy (>3-fold) in FLG mutation carriers with higher dust exposure.
- No significant effect of exposure in children without FLG mutations.
Conclusions:
- Early-life environmental peanut exposure increases peanut allergy risk in children with FLG mutations.
- Supports the transcutaneous sensitization hypothesis for peanut allergy development in those with impaired skin barriers.
Background:
Filaggrin (FLG) loss-of-function mutations lead to an impaired skin barrier associated with peanut allergy. Household peanut consumption is associated with peanut allergy, and peanut allergen in household dust correlates with household peanut consumption.
Objective:
We sought to determine whether environmental peanut exposure increases the odds of peanut allergy and whether FLG mutations modulate these odds.
Methods:
Exposure to peanut antigen in dust within the first year of life was measured in a population-based birth cohort. Peanut sensitization and peanut allergy (defined by using oral food challenges or component-resolved diagnostics [CRD]) were assessed at 8 and 11 years. Genotyping was performed for 6 FLG mutations.
Results:
After adjustment for infantile atopic dermatitis and preceding egg skin prick test (SPT) sensitization, we found a strong and significant interaction between natural log (ln [loge]) peanut dust levels and FLG mutations on peanut sensitization and peanut allergy. Among children with FLG mutations, for each ln unit increase in the house dust peanut protein level, there was a more than 6-fold increased odds of peanut SPT sensitization, CRD sensitization, or both in children at ages 8 years, 11 years, or both and a greater than 3-fold increased odds of peanut allergy compared with odds seen in children with wild-type FLG. There was no significant effect of exposure in children without FLG mutations. In children carrying an FLG mutation, the threshold level for peanut SPT sensitization was 0.92 microg of peanut protein per gram (95% CI, 0.70-1.22 microg/g), that for CRD sensitization was 1.03 microg/g (95% CI, 0.90-1.82 microg/g), and that for peanut allergy was 1.17 microg/g (95% CI, 0.01-163.83 microg/g).
Conclusion:
Early-life environmental peanut exposure is associated with an increased risk of peanut sensitization and allergy in children who carry an FLG mutation. These data support the hypothesis that peanut allergy develops through transcutaneous sensitization in children with an impaired skin barrier.
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