BackgroundAdolescents exposed to victimization are at an increased risk for a variety of adverse mental health outcomes, including depressive symptoms. Yet, the biological pathways underlying these associations remain poorly understood. Focusing on within‐person processes, we examined whether low‐grade systemic inflammation mediated the longitudinal associations between peer victimization and depressive symptoms in adolescence.Methods207 adolescents (at baseline Mage = 12.69 years; SD = 0.49; 43.5% female) participated in a multi‐wave longitudinal study, with assessments repeated every 6 months over 1.5 years. At each assessment wave, participants self‐reported their peer victimization experiences and depressive symptoms. Dried blood spots were collected at each wave using a finger prick procedure to assay a key marker of low‐grade systemic inflammation, interkeukin‐6 (IL‐6). Data were analyzed using random‐intercept cross‐lagged panel models.ResultsThe cross‐lagged paths from IL‐6 to depressive symptoms were significant across all models and waves (β12 = .13; β23 = .12; β34 = .08), indicating that when adolescents' levels of low‐grade systemic inflammation were above their person‐specific average, they reported increased levels of depressive symptoms in the subsequent months. However, no significant cross‐lagged within‐person associations emerged between peer victimization and either IL‐6 or depressive symptoms.ConclusionsThe findings provide no evidence for the hypothesized mediating role of inflammation in the within‐person associations between peer victimization and depressive symptoms. Nevertheless, they extend prior research by indicating that elevated levels of low‐grade systemic inflammation predict the development of depressive symptoms in adolescence.

中文翻译：

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将全身性炎症作为将同伴受害与青春期抑郁症状联系起来的途径


背景暴露于受害的青少年发生各种不良心理健康结果的风险增加，包括抑郁症状。然而，人们对这些关联的生物学途径仍然知之甚少。专注于人内过程，我们检查了低度全身炎症是否介导了同伴受害与青春期抑郁症状之间的纵向关联。方法207 名青少年 （基线时 Mage = 12.69 岁;SD = 0.49;43.5% 为女性）参与了一项多波纵向研究，在 1.5 年内每 6 个月重复评估一次。在每一波评估中，参与者自我报告了他们的同伴受害经历和抑郁症状。使用手指点刺程序在每个波次收集干血点，以检测低度全身炎症的关键标志物 interkeukin-6 （IL-6）。使用随机截距交叉滞后面板模型分析数据。结果从 IL-6 到抑郁症状的交叉滞后路径在所有模型和波次中都显著 （β12 = .13; β23 = .12; β34 = .08），表明当青少年的低度全身炎症水平高于其个体特异性平均水平时，他们报告了随后几个月抑郁症状水平的增加。然而，同伴受害与 IL-6 或抑郁症状之间没有出现显着的交叉滞后人内关联。结论这些发现没有为炎症在同伴受害和抑郁症状之间的人体内关联中的假设中介作用提供证据。尽管如此，他们通过表明低度全身炎症水平升高可预测青春期抑郁症状的发展来扩展先前的研究。