Institute for Heath and Sport, Victoria University, Western Centre for Health, Research and Education, Sunshine Hospital, Melbourne, VIC, Australia.
Department of Pediatric Surgery, Pediatric Surgery Research Laboratories, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA.
J Neuroinflammation. 2022 Jan 4;19(1):4. doi: 10.1186/s12974-021-02354-1.
Patients with inflammatory bowel disease (IBD) suffer from depression at higher rates than the general population. An etiological trigger of depressive symptoms is theorised to be inflammation within the central nervous system. It is believed that heightened intestinal inflammation and dysfunction of the enteric nervous system (ENS) contribute to impaired intestinal permeability, which facilitates the translocation of intestinal enterotoxins into the blood circulation. Consequently, these may compromise the immunological and physiological functioning of distant non-intestinal tissues such as the brain. In vivo models of colitis provide evidence of increased blood-brain barrier permeability and enhanced central nervous system (CNS) immune activity triggered by intestinal enterotoxins and blood-borne inflammatory mediators. Understanding the immunological, physiological, and structural changes associated with IBD and neuroinflammation may aid in the development of more tailored and suitable pharmaceutical treatment for IBD-associated depression.
炎症性肠病（IBD）患者的抑郁发病率高于普通人群。理论上，中枢神经系统的炎症是导致抑郁症状的一个病因。人们认为，肠道炎症加剧和肠神经系统功能障碍会导致肠道通透性受损，从而使肠道内毒素更容易转移到血液循环中。因此，这些毒素可能会损害大脑等远离肠道的非肠道组织的免疫和生理功能。结肠炎的体内模型提供了证据，表明肠道内毒素和血源性炎症介质会引发血脑屏障通透性增加和中枢神经系统（CNS）免疫活性增强。了解与 IBD 和神经炎症相关的免疫学、生理学和结构变化，可能有助于开发更有针对性和更合适的针对 IBD 相关抑郁症的药物治疗方法。
