The causal associations of inflammatory cytokines with obesity and systemic lupus erythematosus: A Mendelian randomization study

Jun 4, 2024International journal of rheumatic diseases

How inflammatory proteins may be linked to obesity and lupus using genetic analysis

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Abstract

Obesity was associated with 25 cytokines, including CTACK and IL-18, which may play intermediary roles in the relationship to systemic lupus erythematosus (SLE).

Three cytokines, CTACK, IL-18, and SCGFb, were found to be associated with SLE in relation to obesity.
CTACK showed an odds ratio of 1.19, indicating a potential increase in SLE risk with obesity.
IL-18 had an odds ratio of 1.13, suggesting a similar association.
SLE was associated with 18 cytokines, including IP-10 and MIP-1B, which may influence obesity.
Both IP-10 and MIP-1B showed a negative association with obesity, indicating a potential protective effect.

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OBJECTIVE: Previous studies have partly discussed the roles of inflammatory cytokines in obesity and systemic lupus erythematosus (SLE), but the causal relationship among inflammatory cytokines, obesity, and SLE is unclear. It is challenging to comprehensively evaluate the causal relationship between these variables. This study aimed to investigate the role of cytokines as intermediates between obesity and SLE.

METHODS: The inverse-variance weighted method (IVW) of mendelian randomization (MR) is mainly used to explore the causal relationship between exposure and outcome by using the genetic variation of the open large genome-wide association studies (GWAS), namely single-nucleotide polymorphisms (SNPs) related to obesity (more than 600 000 participants), inflammatory cytokines (8293 healthy participants) and SLE (7219 cases). Methods such as weighted median, MR-Egger are used to evaluate the reliability of causality. Reverse analysis is performed for each MR analysis to avoid reverse causality. Cochran's Q statistic and funnel chart are used to detect heterogeneity, MR-Egger intercept test and leave-one-out sensitivity analyses evaluated pleiotropy.

RESULTS: Obesity was associated with 25 cytokines, and 3 cytokines were associated with SLE, including CTACK (OR = 1.19, 95% CI: 1.06, 1.33, p = .002), IL-18 (OR = 1.13, 95% CI: 1.01, 1.26, p = .027), SCGFb (OR = 0.89, 95% CI: 0.79, 0.99, p = .044). In the opposite direction, SLE was associated with 18 cytokines, and 2 cytokines were associated with obesity, including IP-10 (β = -.03, 95% CI: -0.05, -0.01, p = .002), MIP-1B (β = -.03, 95% CI: -0.05, -0.01, p = .004). IVW IVW

CONCLUSION: Our MR study suggested that CTACK, IL-18 and SCGFb may play an intermediary role in obesity to SLE, while IP-10 and MIP-1B may play an intermediary role in SLE to obesity.

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The causal associations of inflammatory cytokines with obesity and systemic lupus erythematosus: A Mendelian randomization study

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