Dysregulated kynurenine (KYN) pathway has been implicated in the pathophysiology of depression. In this systematic review, we examined the relationship between kynurenine pathway metabolites (KYN, kynurenic acid KYNA, tryptophan TRP, quinolinic acid QUIN, KYN/TRP ratio) and depression symptoms in the context of pro-inflammatory activation and immune response. Out of 5,082 articles, fifteen studies were suitable; ten studies (N = 315 medically ill patients treated with interferon-alpha IFN-α) reported baseline and post-intervention plasma KYN, TRP and KYN/TRP ratios which were included in quantitative meta-analysis. Data from five studies were summarized (IFN-α, interferon-beta IFN-β, and lipopolysaccharide LPS). We found that IFN-α treatment in patients with chronic illnesses was associated with decreased TRP, increased levels of KYN and KYN/TRP ratio and depression scores from baseline to follow-up at both 4 and 24 weeks. Our findings suggest that increased risk of depression observed after immune-activating agents in patients with chronic medical illnesses is likely mediated by the kynurenine pathway. Further prospective studies are required to investigate the exact pathophysiology of the KYN pathway in depression.

失调的犬尿氨酸 (KYN) 通路与抑郁症的病理生理学有关。在这篇系统评价中，我们在促炎激活和免疫反应的背景下检查了犬尿氨酸途径代谢物（KYN、犬尿氨酸 KYNA、色氨酸 TRP、喹啉酸 QUIN、KYN/TRP 比率）与抑郁症状之间的关系。在 5,082 篇文章中，有 15 项研究是合适的；10 项研究（N = 315 名接受干扰素-α IFN-α 治疗的医学疾病患者）报告了基线和干预后血浆 KYN、TRP 和 KYN/TRP 比率，这些比率被纳入定量荟萃分析。总结了五项研究的数据（IFN-α、干扰素-β IFN-β 和脂多糖 LPS）。我们发现慢性病患者的 IFN-α 治疗与 TRP 降低有关，在第 4 周和第 24 周时，从基线到随访的 KYN 和 KYN/TRP 比率和抑郁评分水平均有所增加。我们的研究结果表明，在慢性疾病患者中使用免疫激活剂后观察到的抑郁风险增加可能是由犬尿氨酸途径介导的。需要进一步的前瞻性研究来调查抑郁症 KYN 通路的确切病理生理学。