The Association of Early-life Exposure to Endotoxin and Longitudinal Atopic Dermatitis Phenotypes
Recommended Citation
Daklallah M, Lin C, Sitarik A, Kim H, Wegienka G, Levin A, Cassidy A, Johnson C, Zoratti E, Eapen A. The Association of Early-life Exposure to Endotoxin and Longitudinal Atopic Dermatitis Phenotypes. J Allergy Clin Immunol 2026; 157(2):AB276.
Document Type
Conference Proceeding
Publication Date
2-10-2026
Publication Title
J Allergy Clin Immunol
Keywords
endotoxin, adult, Alzheimer disease, atopic dermatitis, birth cohort, child, cohort analysis, conference abstract, controlled study, female, genotype, human, longitudinal study, major clinical study, male, phenotype
Abstract
Rationale: While endotoxin exposure is protective against childhood atopic dermatitis (AD), less is known about its association with longitudinal AD phenotypes and the effects of endotoxin receptor (CD14) genotype. We sought to investigate associations of early-life endotoxin exposure and longitudinal AD phenotypes. Methods: Endotoxin was measured from living room dust collected from the homes of 416 children enrolled in a birth cohort at age 1-month (N=388) and 6-months (N=367). AD was defined as ever/never (by age 10 years), early-onset (by age 2 years), late-onset (by age 10 years but not at age 2), and persistent (AD at both age 2 and 10 years]. Poisson regression were used to examine dust endotoxin concentrations for associations with AD (ever/never) and multinomial logistic regression were used for longitudinal AD phenotypes, with adjustment for confounders. Analyses was additionally stratified by sex and endotoxin receptor (CD14) genotype (AA, AG, GG). Results: Overall, endotoxin concentrations were not associated with ever AD. When stratified by sex, there was a decrease in the risk of ever AD amongst girls only (aRR[95% CI] =0.90 [0.81, 1.0]; p=0.047) for each 2-fold increase of 1-month endotoxin concentration. For longitudinal AD phenotypes, every 2-fold increase in 1-month endotoxin concentration was associated with decreased early-onset AD amongst girls only (aOR[95% CI]=0.73[0.57, 0.94]; p=0.016). When stratifying by CD14 genotype, for every 2-fold increase in 6-month endotoxin concentration, participants with an AG genotype had lower likelihood of late-onset AD (aOR=0.65[0.46, 0.94]; p=0.021). Conclusions: Child sex and CD14 genotype impact the association of early-life endotoxin exposure and childhood AD phenotypes.
Volume
157
Issue
2
First Page
AB276
