Selective serotonin reuptake inhibitors and inflammatory bowel disease; Beneficial or malpractice
Open accessAbstract
IBD, a chronic inflammatory disease, has been manifested as a growing health problem. No Crohn's and Colitis councils have officially ratified anti-depressants as a routine regimen for IBD patients. However, some physicians empirically prescribe them to rectify functional bowel consequences such as pain and alleviate psychiatric comorbidities. On the other side, SSRIs' prescription is accompanied by adverse effects such as sleep disturbances. Prolonged intermittent hypoxia throughout sleep disturbance such as sleep apnea provokes periodic reductions in the partial oxygen pressure gradient in the gut lumen. It promotes gut microbiota to dysbiosis, which induces intestinal inflammation. This phenomenon and evidence representing the higher amount of serotonin associated with Crohn's disease challenged our previous knowledge. Can SSRIs worsen the IBD course? Evidence answered the question with the claim on anti-inflammatory properties (central and peripheral) of SSRIs and illuminated the other substantial elements (compared to serotonin elevation) responsible for IBD pathogenesis. However, later clinical evidence was not all in favor of the benefits of SSRIs. Hence, in this review, the molecular mechanisms and clinical evidence are scrutinized and integrated to clarify the interfering molecular mechanism justifying both supporting and disproving clinical evidence. Biphasic dose-dependent serotonin behavior accompanying SSRI shifting function when used up for the long-term can be assumed as the parameters leading to IBD patients' adverse outcomes. Despite more research being needed to elucidate the effect of SSRI consumption in IBD patients, periodic prescriptions of SSRIs at monthly intervals can be recommended.
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Release of pro-inflammatory cytokines including IL1, IL6, and TNF, as well as chemokines, results in recruitment of immune cells.
“The release of pro-inflammatory cytokines, including interleukin (IL) 1, IL6, and tumor necrosis factor (TNF), as well as chemokines, results in the recruitment of immune cells [39, 40].”
From Immunogenicity of decellularized extracellular matrix scaffolds: a bottleneck in tissue engineering and regenerative medicine (2023) · cites this paper as [40]
Section 4.2 (page unavailable) reports that reduced IL-1β, IL-6, and TNF-α expression accompanied suppressed immune-cell recruitment in a rat model. It also mentions IL-8/CXCL8, but does not state that release of those cytokines and chemokines causes immune-cell recruitment. (LLM, conf=0.78)
Experimental — accuracy not yet measuredAfter recognition by PRRs, DAMPs promote transcription of genes contributing to inflammation.
“After recognition by PRRs, DAMPs promote the transcription of genes contributing to the inflammation process.”
From Immunogenicity of decellularized extracellular matrix scaffolds: a bottleneck in tissue engineering and regenerative medicine (2023) · cites this paper as [40]
Section 4.3 says DAMPs are recognized by PRRs on immune cells and that PRR signaling can induce inflammation. It does not state that DAMP recognition promotes transcription of inflammation-related genes; that specific mechanism is unsupported by our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measured
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- Authors
- Hatamnejad, M. R., Baradaran Ghavami, S., Shirvani, M., Asghari Ahmadabad, M., Shahrokh, S., Farmani, M., Sherkat, G., Asadzadeh Aghdaei, H., & Zali, M. R.
- Affiliations
- Research Institute for Gastroenterology and Liver Diseases (IR)
- Shiraz University of Medical Sciences (IR)
- Islamic Azad University, Mashhad (IR)
- Corresponding author
- Shahrokh, Shabnam
- Venue
- Frontiers in Immunology
- Publisher
- Frontiers Media SA
- Published
- 2022-10-06
- Volume
- 13
- Pages
- 980189-980189
- ISSN
- 1664-3224 (ISSN-L)
- PMC
- PMC9583131
- OpenAlex
- W4302287274
- Cited by
- 28
- References
- 151
- Citations by year
- 2026: 3 · 2025: 10 · 2024: 8 · 2023: 6 · 2022: 1
- FWCI
- 0.96
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Immunology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Keywords
- selective serotonin reuptake inhibitors, inflammatory bowel disease, Crohn's disease, ulcerative colitis, serotonin, gut dysbiosis, sleep disorders, sleep apnea, intermittent hypoxia, intestinal inflammation, psychiatric comorbidity, adverse drug reactions
- MeSH terms
- Crohn Disease, Humans, Malpractice, Oxygen, Serotonin, Inflammatory Bowel Diseases, Selective Serotonin Reuptake Inhibitors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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