A wealth of evidence has implicated inflammation in the development of depression. Yet, the heterogeneous nature of depression has impeded efforts to understand, prevent, and treat the disease. The purpose of this integrative review is to summarize the connections between inflammation and established core features of depression that exhibit more homogeneity than the syndrome itself: exaggerated reactivity to negative information, altered reward processing, decreased cognitive control, and somatic syndrome. For each core feature, we first provide a brief overview of its relevance to depression and neurobiological underpinnings, and then review evidence investigating a potential role of inflammation. We focus primarily on findings from experimental paradigms of exogenously-induced inflammation. We conclude that inflammation likely plays a role in exaggerated reactivity to negative information, altered reward reactivity, and somatic symptoms. There is less evidence supporting an effect of inflammation on cognitive control as assessed by standard neuropsychological measures. Finally, we discuss implications for future research and recommendationsfor how to test the role of inflammation in the pathogenesis of heterogeneous psychiatric disorders.

大量证据表明炎症与抑郁症的发展有关。然而，抑郁症的异质性阻碍了理解、预防和治疗该疾病的努力。本综合综述的目的是总结炎症与抑郁症的既定核心特征之间的联系，这些特征比综合征本身表现出更多的同质性：对负面信息的过度反应、奖励处理的改变、认知控制的降低和躯体综合征。对于每个核心特征，我们首先简要概述其与抑郁症和神经生物学基础的相关性，然后回顾调查炎症潜在作用的证据。我们主要关注外源性炎症实验范式的发现。我们得出的结论是，炎症可能在对负面信息的过度反应、奖赏反应改变和躯体症状中发挥作用。通过标准神经心理学测量评估，支持炎症对认知控制的影响的证据较少。最后，我们讨论了对未来研究的影响以及如何测试炎症在异质性精神疾病发病机制中的作用的建议。