Observational studies have revealed an association between certain inflammatory cytokines and the occurrence of Sensorineural Hearing Loss (SNHL), but the causal relationship remains unclear. We conducted a two-sample Mendelian randomization (MR) analysis to assess the causal effects of 23 inflammatory cytokines on the risk of SNHL. For the exposure data, we collected genetic variants associated with inflammatory cytokines as instrumental variables (IVs) from a meta-analysis of genome-wide association studies (GWAS) in Finland (with a sample size of up to 293,17). For the outcome data, we obtained summary data for ischemic stroke from a large-scale GWAS meta-analysis involving 34 studies (including 15,952 cases and 196,592 controls). Further, a series of sensitivity analyses were performed to validate the main MR results. Based on the main MR estimates and additional sensitivity analyses, we established a robust association after Bonferroni correction: the odds ratio (95% CI) per unit change in genetically increased IL-2 was 1.254 (1.002-1.570) for SNHL. The chemokine MIP1b showed a nominal significant association with the risk of SNHL (OR = 0.828, 95% CI: 0.732-0.937, P = 0.003). There was no evidence to suggest a causal effects between other inflammatory cytokines and the risk of SNHL. The present study proposed a potential causal relationship between IL-2, MIP1b and SNHL, providing new insights into potential therapeutic targets for SNHL.