Abstract
Previous studies have highlighted the correlation between inflammatory responses and vestibular neuritis (VN). The aim of Mendelian randomization was to assess the causal associations between 91 inflammatory proteins and vestibular neuritis comprehensively. By leveraging publicly accessible genetic datasets, we probed whether 91 inflammatory proteins serve as upstream determinants of vestibular neuritis. We conducted a comprehensive sensitivity analysis to assess the robustness, heterogeneity, and polygenicity of our findings. Three inflammatory proteins were found to exert a significant causal effect on the VN: eotaxin levels are associated with a reduced risk of VN (inverse variance weighting [IVW]: odds ratio [OR] = 0.7113, 95% confidence intervals [CI] = 0.5199-0.9731, P = .0331). Similarly, the measurement of monocyte chemotactic protein-2 is linked to a decreased risk of VN (IVW: OR = 0.8535, 95% CI = 0.7328-0.9942, P = .0418). Conversely, an increase in the level of the T-cell surface glycoprotein CD5 is correlated with an increased risk of VN (IVW: OR = 1.3969, 95% CI = 1.0095-1.9331, P = .0437). This study suggested that eotaxin, monocyte chemotactic protein-2, and the T-cell surface glycoprotein CD5 may play crucial roles in the pathogenesis of VN. The potential use of these inflammatory proteins for diagnosing VN or as therapeutic targets has significant clinical implications.