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<p>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 (<i>P</i> = 0.007), elevated IL-19 levels (<i>P</i> = 0.014), and an increased IL-19/IL-10 (<i>P</i> &lt; 0.001). Serum IL-10 levels in AOS patients were significantly negatively correlated with PANSS negative factor scores (<i>r</i> = −0.254, <i>P</i> = 0.020) and excitement/hostility factor scores (<i>r</i> = −0.348, <i>P</i> = 0.001), while the IL-19/IL-10 was positively correlated with excitement/hostility factor scores (<i>r</i> = 0.349, <i>P</i> = 0.001). Exploratory stratified analyses revealed significant negative correlations between IL-10 and excitement/hostility factor in both male patients (<i>r</i> = −0.432, <i>P</i> = 0.010) and female patients (<i>r</i> = −0.375, <i>P</i> = 0.009). Additionally, lower IL-10 levels were an independent predictor of AOS (RR = 0.808, 95%CI: 0.714–0.914, <i>P</i> = 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.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月9日

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  • Haidong Yang,
  • Zhihui Shi,
  • Li Xu,
  • Chenchen Xu,
  • Jing Li,
  • Lingshu Luan,
  • Tingting Jin,
  • Xiaobin Zhang

摘要

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.