Fields Christopher T, Chassaing Benoit, de Vries Geert J
Department of Psychiatry, Yale University, New Haven, CT, 06519, United States.
Inserm U1016, Team "Mucosal Microbiota in Chronic Inflammatory Diseases", Université de Paris, CNRS UMR 8104, 75014 Paris, France.
Med Hypotheses. 2022 Apr;161. doi: 10.1016/j.mehy.2022.110799. Epub 2022 Feb 14.
To date, much of the focus of gut-brain axis research has been on gut microbiota regulation of anxiety and stress-related behaviors. Much less attention has been directed to potential connections between gut microbiota and compulsive behavior. Here, we discuss a potential link between gut barrier dysfunction and compulsive behavior that is mediated through "type 2" rather than "type 1" inflammation. We examine connections between compulsive behavior and type 2 inflammation in Tourette syndrome, obsessive-compulsive disorder, autism, addiction, and post-traumatic stress disorder. Next, we discuss potential connections between gut barrier dysfunction, type 2 inflammation, and compulsive behavior. We posit a potential mechanism whereby gut barrier dysfunction-associated type 2 inflammation may drive compulsive behavior through histamine regulation of dopamine neurotransmission. Finally, we discuss the possibility of exploiting the greater accessibility of the gut relative to the brain in identifying targets to treat compulsive behavior disorders.
迄今为止，肠道-脑轴研究的大部分焦点都集中在肠道微生物群对焦虑和应激相关行为的调节上。而对于肠道微生物群与强迫行为之间的潜在联系，关注则少得多。在此，我们讨论肠道屏障功能障碍与强迫行为之间的一种潜在联系，这种联系是通过“2型”而非“1型”炎症介导的。我们研究了图雷特综合征、强迫症、自闭症、成瘾和创伤后应激障碍中强迫行为与2型炎症之间的联系。接下来，我们讨论肠道屏障功能障碍、2型炎症和强迫行为之间的潜在联系。我们提出了一种潜在机制，即肠道屏障功能障碍相关的2型炎症可能通过组胺对多巴胺神经传递的调节来驱动强迫行为。最后，我们讨论了利用肠道相对于大脑更容易接近这一特点来确定治疗强迫行为障碍靶点的可能性。
