MicroRNA‐146a and microRNA‐146b deficiency correlates with exacerbated disease activity, and their longitude increment relates to etanercept response in psoriasis patients

Abstract

BackgroundMicroRNA (miR)‐146a and miR‐146b regulate autoimmunity, inflammation, and keratinocytes proliferation to engage in psoriasis pathology. The current study aimed to investigate their correlation with disease risk and clinical features, and the linkage of their longitudinal changes with clinical response to etanercept in psoriasis patients.MethodsPlasma samples were collected from 84 moderate‐to‐severe psoriasis patients who underwent etanercept treatment (at baseline (M0), 1 month (M1), 3 months (M3), and 6 months (M6)), 80 disease controls and 80 health controls (both after enrollment); afterward, miR‐146a and miR‐146b expressions were detected by RT‐qPCR. Furthermore, PASI75 and PASI90 responses were assessed in psoriasis patients.ResultsBoth miR‐146a and miR‐146b were decreased in psoriasis patients compared with disease controls and health controls (all p < 0.001), which also distinguished psoriasis patients from disease controls and health controls by receiver‐operating characteristic analyses. Furthermore, miR‐146a positively correlated with miR‐146b in psoriasis patients (p < 0.001) and disease controls (p = 0.005) but not in healthy controls (p = 0.062). In psoriasis patients, miR‐146a negatively related to psoriatic body surface area (p = 0.011) and PASI score (p = 0.003); miR‐146b negatively linked with PASI score (p = 0.020). At M1, M3, and M6 after etanercept treatment, PASI75 response rate was 14.3%, 32.1%, and 69.0%, respectively; PASI90 response rate was 1.2%, 17.9%, and 36.9%, respectively. During etanercept treatment, both miR‐146a and miR‐146b elevated gradually over time and their longitude increments were associated with PASI75 response (all p < 0.001).ConclusionMiR‐146a and miR‐146b might serve as indicators for optimizing etanercept application and improving treatment outcomes in psoriasis patients.