BACKGROUND Depression rates increase markedly for girls across the adolescent transition, but the social-environmental and biological processes underlying this phenomenon remain unclear. To address this issue, we tested a key hypothesis from Social Signal Transduction Theory of Depression, which posits that individuals who mount stronger inflammatory responses to social stress should exhibit greater increases in depressive symptoms following interpersonal life stress exposure than those who mount weaker inflammatory responses to such stress. METHOD Participants were 116 adolescent girls (Mage  = 14.71) at risk for psychopathology, defined as having a history of mental health concerns (e.g., psychiatric treatment, significant symptoms) over the past 2 years. At baseline, we characterized their inflammatory reactivity to social stress by quantifying their salivary proinflammatory cytokine responses to a laboratory-based social stressor. Then, 9 months later, we assessed the interpersonal and noninterpersonal stressful life events that they experienced over the prior 9 months using an interview-based measure of life stress. RESULTS As hypothesized, greater interpersonal life stress exposure was associated with significant increases in depression over time, but only for girls exhibiting stronger salivary tumor necrosis factor-α and interleukin-1β reactivity to social stress. In contrast, noninterpersonal stress exposure was unrelated to changes in depression longitudinally, both alone and when combined with youths' cytokine reactivity scores. DISCUSSION These results are consistent with Social Signal Transduction Theory of Depression and suggest that heightened inflammatory reactivity to social stress may increase adolescents' risk for depression. Consequently, it may be possible to reduce depression risk by modifying inflammatory responses to social stress.

中文翻译：

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青春期的人际生活压力、炎症和抑郁：测试抑郁症的社会信号转导理论。

背景 在整个青春期过渡期间，女孩的抑郁率显着增加，但这种现象背后的社会环境和生物学过程仍不清楚。为了解决这个问题，我们测试了来自抑郁症社会信号转导理论的一个关键假设，该假设假设对社会压力产生更强炎症反应的个体在人际生活压力暴露后的抑郁症状应该比那些对社会压力产生较弱炎症反应的个体表现出更大的抑郁症状增加。这样的压力。方法 参与者是 116 名青春期女孩 (Mage = 14.71)，有精神病理学风险，定义为在过去 2 年内有心理健康问题（例如，精神病治疗、显着症状）的病史。在基线时，我们通过量化他们对基于实验室的社会压力源的唾液促炎细胞因子反应来描述他们对社会压力的炎症反应。然后，9 个月后，我们使用基于访谈的生活压力测量方法评估了他们在过去 9 个月中经历的人际和非人际压力生活事件。结果正如假设的那样，随着时间的推移，更大的人际生活压力暴露与抑郁症的显着增加有关，但仅适用于对社会压力表现出更强的唾液肿瘤坏死因子-α和白细胞介素-1β反应性的女孩。相比之下，非人际压力暴露与抑郁症的纵向变化无关，无论是单独还是与青少年的细胞因子反应评分相结合。讨论 这些结果与抑郁症的社会信号转导理论一致，表明对社会压力的炎症反应增强可能会增加青少年患抑郁症的风险。因此，有可能通过改变对社会压力的炎症反应来降低抑郁风险。