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Inflammatory factors mediated the effect of air pollution on ischemic stroke: a two-step, mediation Mendelian
1Department of Neurology, Changde Hospital, Xiangya School of Medicine, Central South University, Changde, China. zhujm0718@126.com.
Objective:
Numerous investigations have indicated a correlation between air pollution (AP) and an elevated ischemic stroke (IS) likelihood. The existing literature does not provide a consensus about the possible link between AP and IS. A two-sample Mendelian randomization (MR) analysis was utilized to systematically measure the causal link between AP and ischemic stroke. Furthermore, the mediating impact of inflammatory factors was also performed by a two-step MR.
Materials And Methods:
A two-sample MR analysis was utilized to examine the AP impact on the incidence of IS. Additionally, a two-step MR approach was carried out to account for possible mediating variables. The indirect impact was determined by employing the product approach, which included multiplying the AP impact on inflammatory factors by the inflammatory factors' impacts on IS. The MR effect was identified through inverse variance-weighted (IVW) meta-analysis of each Wald Ratio. Additionally, complementary studies were conducted using the weighted median and MR-egger approaches.
Results:
The IVW method with random effects showed that the per unit increase in genetically predicted PM2.5 was linked to the 0.362-fold elevated ischemic stroke risk (OR: 1.362, 95% CI: 1.032-1.796, p=0.029). Furthermore, the IVM technique, incorporating random effects, demonstrated that the per unit increase in genetically predicted PM2.5 was related to an elevated Interleukin (IL)-1β risk (OR: 1.529, 95% CI: 1.191-1.963, p=0.001), IL-6 (OR: 1.498, 95% CI: 1.094-2.052, p=0.012) and IL-17 (OR: 1.478, 95% CI: 1.021-2.139, p=0.038). IL-1β, IL-6, and IL-17 modulated the PM2.5 impact on ischemic stroke, while the proportion mediated by them was 59.5%.
Conclusions:
A positive correlation between genetically predicted PM2.5 levels and elevated ischemic stroke risk is mediated by IL-1β, IL-6, and IL-17.
Insights
Exposure to fine particulate matter (PM2.5) air pollution increases ischemic stroke risk. This risk is mediated by inflammatory factors like Interleukin-1 beta, Interleukin-6, and Interleukin-17.
Area of Science:
- Environmental Health
- Epidemiology
- Genetics
Background:
- Air pollution (AP) is linked to increased ischemic stroke (IS) risk, but consensus is lacking.
- Investigating the causal relationship and mediating factors is crucial for public health.
Approach:
- A two-sample Mendelian randomization (MR) analysis was employed to assess the causal effect of AP on IS.
- A two-step MR approach quantified the mediating role of inflammatory factors (IL-1β, IL-6, IL-17).
- Inverse variance-weighted (IVW) meta-analysis, weighted median, and MR-Egger methods were used for robust analysis.
Key Points:
- Genetically predicted PM2.5 exposure significantly increased IS risk (OR: 1.362, p=0.029).
- PM2.5 exposure was associated with elevated Interleukin-1 beta (OR: 1.529, p=0.001), Interleukin-6 (OR: 1.498, p=0.012), and Interleukin-17 (OR: 1.478, p=0.038) levels.
- Inflammatory factors IL-1β, IL-6, and IL-17 mediated 59.5% of the PM2.5 effect on IS.
Conclusions:
- Genetically predicted PM2.5 levels causally increase ischemic stroke risk.
- Interleukin-1 beta, Interleukin-6, and Interleukin-17 are key mediators in the PM2.5-ischemic stroke pathway.
- Targeting inflammation may be a viable strategy to mitigate ischemic stroke risk from air pollution.
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