Understanding immunological origins of atopic dermatitis through multi-omic analysis.
allergy
atopic dermatitis
atopy
biomarkers
cytokines
eczema
microbiome
oropharynx
saliva
Journal
Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology
ISSN: 1399-3038
Titre abrégé: Pediatr Allergy Immunol
Pays: England
ID NLM: 9106718
Informations de publication
Date de publication:
06 2022
06 2022
Historique:
revised:
19
05
2022
received:
04
03
2022
accepted:
30
05
2022
entrez:
27
6
2022
pubmed:
28
6
2022
medline:
29
6
2022
Statut:
ppublish
Résumé
The pathophysiology of atopic dermatitis (AD) is multifactorial, impacted by individual medical, demographic, environmental, and immunologic factors. This study used multi-omic analyses to assess how host and microbial factors could contribute to infant AD development. This longitudinal cohort study included 129 term infants, identified as AD (n = 37) or non-AD (n = 92) using the Infant Feeding Practices-II survey and review of medical records. Standardized surveys were used to assess medical and demographic traits (gestational age, sex, race, maternal AD, and atopy family history), and environmental exposures (delivery method, maternal tobacco use, pets, breastfeeding duration, and timing of solid food introduction). Saliva was collected at 6 months for multi-omic assessment of cytokines, microRNAs, mRNAs, and the microbiome. The contribution of each factor to AD status was assessed with logistic regression. Medical, demographic, and environmental factors did not differ between AD and non-AD infants. Five "omic" factors (IL-8/IL-6, miR-375-3p, miR-21-5p, bacterial diversity, and Proteobacteria) differed between groups (p < .05). The severity of AD was positively associated with levels of miR-375-3p (R = .17, p = .049) and Proteobacteria (R = .22, p = .011), and negatively associated with levels of miR-21-5p (R = .20, p = .022). Multi-omic features accounted for 17% of variance between groups, significantly improving an AD risk model employing medical, demographic, and environmental factors (X Interactions between the microbiome and host signaling may predispose certain infants to AD by promoting a pro-inflammatory environment.
Sections du résumé
BACKGROUND
The pathophysiology of atopic dermatitis (AD) is multifactorial, impacted by individual medical, demographic, environmental, and immunologic factors. This study used multi-omic analyses to assess how host and microbial factors could contribute to infant AD development.
METHODS
This longitudinal cohort study included 129 term infants, identified as AD (n = 37) or non-AD (n = 92) using the Infant Feeding Practices-II survey and review of medical records. Standardized surveys were used to assess medical and demographic traits (gestational age, sex, race, maternal AD, and atopy family history), and environmental exposures (delivery method, maternal tobacco use, pets, breastfeeding duration, and timing of solid food introduction). Saliva was collected at 6 months for multi-omic assessment of cytokines, microRNAs, mRNAs, and the microbiome. The contribution of each factor to AD status was assessed with logistic regression.
RESULTS
Medical, demographic, and environmental factors did not differ between AD and non-AD infants. Five "omic" factors (IL-8/IL-6, miR-375-3p, miR-21-5p, bacterial diversity, and Proteobacteria) differed between groups (p < .05). The severity of AD was positively associated with levels of miR-375-3p (R = .17, p = .049) and Proteobacteria (R = .22, p = .011), and negatively associated with levels of miR-21-5p (R = .20, p = .022). Multi-omic features accounted for 17% of variance between groups, significantly improving an AD risk model employing medical, demographic, and environmental factors (X
CONCLUSION
Interactions between the microbiome and host signaling may predispose certain infants to AD by promoting a pro-inflammatory environment.
Substances chimiques
MicroRNAs
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e13817Informations de copyright
© 2022 EAACI and John Wiley and Sons A/S. Published by John Wiley and Sons Ltd.
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