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Exploring lipidome mediated inflammatory pathways in acute pancreatitis using mendelian randomization.
Wenbin Liu1, Song Yang1, Yuhan Li2
1Department of Emergency, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Scientific Reports
|January 8, 2025
Summary
Certain lipid species, like specific phosphatidylcholines and sterol esters, may protect against acute pancreatitis (AP) by reducing inflammation. Conversely, phosphatidylinositol may increase AP risk through inflammatory pathways.
Area of Science:
- Genetics and Genomics
- Gastroenterology
- Metabolomics
Background:
- Acute pancreatitis (AP) is a severe gastrointestinal disease with rising hyperlipidemic causes.
- Understanding the causal links between lipids, inflammation, and AP is crucial for developing new treatments.
Purpose of the Study:
- To investigate the potential causal relationships between lipidome profiles, inflammatory mediators, and the risk of acute pancreatitis.
- To identify specific lipid species and inflammatory factors influencing AP development.
Main Methods:
- Utilized a two-sample, bidirectional Mendelian randomization approach.
- Analyzed genetic variants in a large cohort of 10,630 AP cases and 844,679 controls.
- Accounted for heterogeneity, pleiotropy, and potential reverse causation.
Main Results:
- Identified 23 lipid species with unidirectional causal effects on AP risk.
- Five inflammatory factors (CD5, IL-13, MMP-1, STAMBP, TNFRSF9) showed potential causal links to AP.
- Sterol ester (27:1/20:4) and several phosphatidylcholines demonstrated a protective effect against AP, mediated by reduced STAMBP and MMP-1 levels.
- Phosphatidylinositol (16:0_18:1) was associated with increased AP risk, potentially via elevated MMP-1 and STAMBP.
Conclusions:
- Specific lipid metabolites, particularly phosphatidylcholines and sterol esters, may play a protective role in AP by modulating inflammatory responses.
- Phosphatidylinositol may exacerbate AP risk by promoting inflammation.
- Mendelian randomization is a valuable tool for uncovering causal links in AP pathogenesis.
- Further research is needed to explore molecular mechanisms and translational applications for AP prevention and treatment.
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