Neuroinflammation as an etiological trigger for depression comorbid with inflammatory bowel disease
Open accessAbstract
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.
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The relationship between IBD and mental illness can be bidirectional, with systemic inflammation and gut-brain interactions as possible mechanisms.
“Recent studies indicate that the relationship between IBD and mental illness can be bidirectional, evoking the systemic inflammation that damages the body’s immune and nervous systems and is a possible mechanism for both IBD and mental illness, as well as complex gut–brain interactions [46,47,48,49].”
From Association between Childhood Onset Inflammatory Bowel Disease and Psychiatric Comorbidities in Adulthood (2023) · cites this paper as [46]
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- Authors
- Craig, C. F., Filippone, R. T., Stavely, R., Bornstein, J. C., Apostolopoulos, V., & Nurgali, K.
- Affiliations
- Sunshine Hospital (AU)
- Harvard University (US)
- The University of Melbourne (AU)
- Australian Institute for Musculoskeletal Science (AU)
- Corresponding author
- Nurgali, Kulmira
- Venue
- Journal of Neuroinflammation
- Published
- 2022-01-04
- Volume
- 19
- Issue
- 1
- Pages
- 4-4
- ISSN
- 1742-2094 (ISSN-L)
- PMC
- PMC8729103
- OpenAlex
- W4206422593
- Cited by
- 124
- References
- 373
- Citations by year
- 2026: 26 · 2025: 39 · 2024: 30 · 2023: 20 · 2022: 9
- FWCI
- 1.85
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Journal of Neuroinflammation (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Victoria University Research Repository (Victoria University) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Minerva Access (University of Melbourne) (submittedVersion, cc-by)
- Funders
- Victoria University
- National Health and Medical Research Council (1158952)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- neuroinflammation, depression, inflammatory bowel disease, intestinal permeability, enterotoxin, blood-brain barrier permeability, enteric nervous system, colitis, gut-brain axis
- MeSH terms
- Brain-Gut Axis, Neuroinflammatory Diseases, Depression, Humans, Inflammatory Bowel Diseases
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