Abstract
Previous studies have reported that the occurrence and development of acne are closely associated with immune-inflammatory responses. Mendelian randomization was performed to further assess the causal correlation between 41 inflammatory cytokines and acne. Mendelian two-sample randomization utilized genetic variants for acne from a large open genome-wide association study (1299 cases and 211,139 controls of European ancestry) and inflammatory cytokines from a genome-wide association study abstract containing 8293 healthy participants. The causal relationship between exposure and outcome was explored primarily using an inverse variance weighting approach. In addition, multiple sensitivity analyses including MR-Egger, weighted median, simple model, weighted model, and MR-PRESSO were applied simultaneously to enhance the final results. The results suggest that il-10, MIP-1A, and SCGF-β are suggestive of the risk of acne in clinical practice (OR = 0.799, 95% CI = 0.641-0.995, P = .045; OR = 0.55, 95% CI = 0.388-0.787, P = .001; OR = 1. 152, 95% CI = 1.001-1.325, P = .048). Our study conclusively identified a causal relationship between il-10 and circulating levels of acne risk and a suggestive link between MIP-1A and SCGF-β and acne. Our study may provide greater insight into the pathogenesis of acne and develop effective management strategies for the clinic. We believe that IL-10, MIP-1A, and SCGF-β could be potential therapeutic targets for acne development.