ArticleMedicine2025
The causal relationship between 91 inflammatory cytokines and chronic pancreatitis, and the mediating role of 1400 metabolites.
Article in Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Considerable amounts of studies have confirmed a close relationship between specific inflammatory cytokines and chronic pancreatitis (CP), while the causal effect between the 2 remains unclear. This study is to evaluate the causal relationship between 91 inflammatory cytokines and CP using bidirectional 2-sample Mendelian randomization (MR) method, and to investigate the mediating role of 1400 metabolites through a 2-step MR analysis. Genome wide association study (GWAS) data related to 91 inflammatory cytokines were sourced from 14,824 participants of European populations, and CP related GWAS data from a Finnish database, covering 3875 cases of CP cases and 361,641 controls. A total of 1400 circulating metabolites were derived from 8299 individuals. This study used inverse variance weighted (IVW) as the main analysis method, complemented by 4 other methods. In addition, sensitivity analysis was conducted at different levels, including Cochran Q statistics, MR-egger intercept, MR-PRESSO global test, and "leave-one-out method" (LOO) analysis, ensuring the robustness of the results. The IVW method revealed that levels of CCL23 [OR = 1.120, 95% CI: 1.014-1.237, P = .026], DNER [OR = 1.151, 95% CI: 1.020-1.300, P = .023], IL-6 [OR = 1.240, 95% CI: 1.034-1.486, P = .020], and TNFRSF9 [OR = 1.156, 95% CI: 1.020-1.309, P = .023] increased the CP risk; while CCL19 [OR = 0.902, 95% CI: 0.820-0.991, P = .033], IFN-gamma (IFN-γ) [OR = 0.847, 95% CI: 0.734-0.977, P = .023], IL-10 [OR = 0.853, 95% CI: 0.736-0.988, P = .034], IL-2 [OR = 0.836, 95% CI: 0.719-0.972, P = .020], MCP-3 [OR = 0.879, 95% CI: 0.779-0.993, P = .038] had a protective effect on CP. Although mediation analysis identified 13 metabolites mediating the causal relationships between CCL19, CCL23, IFN-gamma, IL-2, IL-6, MCP-3, and CP, none of these mediating effects achieved statistical significance (P > .05). The 2-sample MR analysis in this study provided convincing evidence for the causal effects of circulating inflammatory cytokines on CP, confirming that CCL23, DNER, IL-6, and TNFRSF9 can increase the CP risk, while CCL19, IFN-gamma, IL-10, IL-2, and MCP-3 reduce the CP risk. The evidence was insufficient to prove a direct mediating role of metabolites in the causal relationship between inflammatory cytokines and CP. This study may contribute to a better understanding of the pathogenesis of CP and improve its prevention and treatment.
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