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Updated: Jun 27, 2026
Measuring Local Anaphylaxis in Mice
Published on: October 14, 2014
Metabolic Biomarkers Mediate Allergic Conjunctivitis via Circulating Inflammatory Proteins: Evidence From a Mendelian
Xiang Cao1,2, Zijiao Xu3,4, Boyang Zhang3,4
1Department of Ophthalmology, Affiliated People's Hospital, Jiangsu University, Zhenjiang, Jiangsu, China.
Purpose:
This study aimed to investigate the mediating role of metabolic biomarkers (MBs) in the association between circulating inflammatory proteins (CIPs) and allergic conjunctivitis (AC) and identify potential therapeutic targets.
Methods:
A Mendelian randomization (MR) study was conducted, leveraging genetic variants as instrumental variables to infer causal relationships. Data were obtained from genome-wide association studies (GWASs), and a two-sample MR was employed to estimate the direct and indirect effects of CIPs on AC through MBs. Inverse-variance weighting (IVW) served as the primary analysis method, supplemented by sensitivity analyses to assess the robustness of findings.
Results:
Six CIPs were found to have significant causal effects on AC. Natural killer cell receptor 2B4 (CD244) exhibited a protective effect, and interleukin-18 receptor 1 (IL-18R1), IL-6, leukemia inhibitory factor (LIF), protein S100-A12 (EN-RAGE), and TNF-related activation-induced cytokine (TRANCE) were identified as risk factors. The MR analysis indicated the mediation role of specific MBs in these associations, with MBs such as 4-oxo-retinoic acid, gulonate, 3-(4-hydroxyphenyl) lactate, S-adenosylhomocysteine, and sphingomyelin, significantly influencing the pathway from CIPs to AC.
Conclusions:
This study highlights the crucial role of MBs in mediating the association between CIPs and AC. These findings offer new insights into the pathophysiology of AC and suggest potential metabolic targets for novel therapeutic approaches.
Translational Relevance:
This study underscores the potential for targeting specific MBs as novel therapeutic approaches to modulate the inflammatory pathways implicated in AC.
