Alterations in serum IL-10 and IL-19 levels in drug-naïve first-episode adolescent-onset schizophrenia and their associations with clinical symptoms

初次发作且未接受药物治疗的青少年精神分裂症患者血清IL-10和IL-19水平的变化及其与临床症状的关系

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Abstract

Immune-inflammatory mechanisms in schizophrenia have received widespread attention, but the levels of interleukin-10 (IL-10) and interleukin-19 (IL-19) and their associations with clinical symptoms in adolescent-onset schizophrenia (AOS) remain unclear. This study aimed to investigate serum IL-10 and IL-19 levels in AOS patients and their relationships with clinical symptoms. This cross-sectional study enrolled 83 drug-naïve first-episode AOS patients and 40 healthy controls. Clinical symptoms were assessed using the Positive and Negative Syndrome Scale (PANSS). Compared with healthy controls, AOS patients exhibited significantly decreased serum IL-10 levels (P = 0.007), elevated IL-19 levels (P = 0.014), and an increased IL-19/IL-10 (P < 0.001). Serum IL-10 levels in AOS patients were significantly negatively correlated with PANSS negative factor scores (r = -0.254, P = 0.020) and excitement/hostility factor scores (r = -0.348, P = 0.001), while the IL-19/IL-10 was positively correlated with excitement/hostility factor scores (r = 0.349, P = 0.001). Exploratory stratified analyses revealed significant negative correlations between IL-10 and excitement/hostility factor in both male patients (r = -0.432, P = 0.010) and female patients (r = -0.375, P = 0.009). Additionally, lower IL-10 levels were an independent predictor of AOS (RR = 0.808, 95%CI: 0.714-0.914, P = 0.001). AOS patients demonstrated an immune imbalance characterized by decreased serum IL-10, elevated IL-19 levels, and an increased IL-19/IL-10. IL-10 levels and the IL-19/IL-10 were closely associated with negative and excitement/hostility symptoms in AOS, with this association exhibiting sex differences. These findings suggest that IL-10 and the pro-inflammatory/anti-inflammatory balance may play an important role in the pathophysiological mechanism of AOS.

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