Neuroinflammation and the Immune-Kynurenine Pathway in Anxiety Disorders.
Neuroinflammation and the Immune-Kynurenine Pathway in Anxiety Disorders.
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焦虑症中的神经炎症和免疫犬尿氨酸通路。
DOI：
10.2174/1570159x15666170913110426
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发表时间：
2018
影响因子：
5.3
通讯作者：
Jeon SW
中科院分区：
文献类型：
--
作者：
Kim YK;Jeon SW
近年来，神经炎症和免疫-犬尿氨酸途径在重度抑郁症（MDD）的心理免疫学领域受到越来越多的关注，而与焦虑障碍相关的研究却非常有限。本研究回顾了应激或炎症通过色氨酸代谢和犬尿氨酸途径调节焦虑的可能机制。通过PubMed的MEDLINE搜索找到相关文献。越来越多的证据表明免疫-犬尿氨酸通路对焦虑的调节作用。犬尿氨酸途径中的色氨酸分解代谢物（TRYCATs）因应激或炎症而失衡，导致血清素和褪黑素缺乏，使焦虑反应更加敏感。此外，TRYCATs通过作为内源性焦虑原或抗焦虑剂、NMDA激动剂或拮抗剂或自由基发生器引起或维持焦虑。我们希望我们对焦虑的心理免疫机制的理解将会扩大，焦虑相关的研究将会得到更多的关注。
Recently, neuroinflammation and the immune-kynurenine pathway have received increased attention in the psychoimmunology field of major depressive disorder (MDD), while studies related to anxiety disorders have been very limited. This study reviewed possible mechanisms by which stress or inflammation modulate anxiety through tryptophan metabolism and the kynurenine pathway. Relevant literature was identified through a search of MEDLINE via PubMed. Accumulating evidence has indicated the modulatory effects of the immune-kynurenine pathway on anxiety. The tryptophan catabolites (TRYCATs) in the kynurenine pathway imbalanced by stress or inflammation induce serotonin and melatonin deficiency, making anxiety reactions more sensitive. In addition, TRYCATs cause or sustain anxiety by acting as endogenous anxiogens or anxiolytics, an NMDA agonist or antagonist, or a free radical generator. We hope that our understanding of the psychoimmunological mechanisms of anxiety will be expanded and anxiety-related studies will receive greater attention.