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Genetic Correlations and Causal Relationships Among Allergic Diseases: A Comprehensive Mendelian Randomization Study
Ping-An Zhang1, Jie-Lin Wang2, Shi-Yan Fu1
1State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, Department of Allergy and Clinical Immunology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China, gzhmc.edu.cn.
Mediators of Inflammation
|April 9, 2026
Summary
This study reveals causal links between allergic diseases like asthma and eczema, identifying novel mediators beyond typical inflammation. These findings offer new therapeutic targets for allergic multimorbidity.
Area of Science:
- Immunology
- Genetics
- Metabolomics
Background:
- Allergic diseases such as allergic asthma (AA), allergic rhinitis (AR), atopic dermatitis (AD), and allergic conjunctivitis (AC) frequently co-occur.
- The precise inflammatory mediators underlying shared allergic disease mechanisms are not well understood.
Purpose of the Study:
- To investigate causal relationships among allergic diseases.
- To identify multiomic mediators contributing to allergic multimorbidity using Mendelian randomization (MR).
Main Methods:
- Analysis of large-scale Genome-Wide Association Study (GWAS) datasets (FinnGen, UK Biobank).
- Application of Linkage Disequilibrium Score Regression (LDSC) and MR-robust adjusted profile scoring (MR-RAPS) for genetic correlation and causal inference.
- Utilized multivariable MR (MVMR) to isolate independent effects, adjusting for type 2 inflammation markers.
- Employed a two-step MR framework to assess mediation by immune cells, metabolites, gut microbiota, and serum proteins.
Main Results:
- Established robust causal links between six pairs of allergic diseases (AA-AR, AA-AD, AR-AA, AR-AD, AD-AA, AD-AR), independent of type 2 inflammation.
- Identified key mediators including granulocyte CD45, pentose acid, Bacteroides intestinalis, and serum proteins ABHD12 and SEZ6L2.
- Pathway analysis implicated cytokine-cytokine receptor interactions and lipid metabolism.
Conclusions:
- Mapped a comprehensive causal network for allergic multimorbidity.
- Discovered novel serum protein and metabolic mediators independent of the type 2 inflammation axis.
- These mediators represent potential therapeutic targets for managing allergic disease crosstalk.
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