Neuroinflammation as an etiological trigger for depression comorbid with inflammatory bowel disease

Journal of Neuroinflammation

Joel C. Bornstein¹  Colin F. Craig²  Rhiannon T. Filippone²  Kulmira Nurgali³  Rhian Stavely⁴  Vasso Apostolopoulos⁵ 

[1] Department of Anatomy and Physiology, The University of Melbourne, Melbourne, Australia;Institute for Heath and Sport, Victoria University, Western Centre for Health, Research and Education, Sunshine Hospital, Melbourne, VIC, Australia;Institute for Heath and Sport, Victoria University, Western Centre for Health, Research and Education, Sunshine Hospital, Melbourne, VIC, Australia;Department of Medicine Western Health, Faculty of Medicine, Dentistry and Health Sciences, The University of Melbourne, Melbourne, VIC, Australia;Regenerative Medicine and Stem Cells Program, Australian Institute of Musculoskeletal Science (AIMSS), Melbourne, VIC, Australia;Institute for Health and Sport, Victoria University, Level 4 Research Labs, Western Centre for Health Research and Education, Sunshine Hospital, 176 Furlong Road, 3021, St Albans, VIC, Australia;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, 02114, Boston, MA, USA;Institute for Heath and Sport, Victoria University, Western Centre for Health, Research and Education, Sunshine Hospital, Melbourne, VIC, Australia;Immunology Program, Australian Institute of Musculoskeletal Science (AIMSS), Melbourne, VIC, Australia;

关键词: Inflammatory bowel disease;    Depression;    Neuroinflammation;    Gut-brain axis;   

DOI  :  10.1186/s12974-021-02354-1

来源: Springer

【 摘 要 】

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.

【 授权许可】

CC BY