Selective serotonin reuptake inhibitors and inflammatory bowel disease; Beneficial or malpractice

Abstract

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.

Comparing chronic obstructive pulmonary disease and depressive disorder in terms of inflammation-related biomarkers

“…High IL-6 levels in rDD patients may reflect the anti-inflammatory pathway of Il-6 signaling. This suggestion can be supported by the fact that the patients included in our study were treated with antidepressants that have anti-inflammatory properties [ 26 ]. Antidepressants have been found to significantly decrease serum soluble IL-6R levels and IL-6 trans-signaling pathways [ 28 ].…”

“…Higher IL-6 levels in rDD may reflect the anti-inflammatory pathway of Il-6 signaling. Patients in our study were treated with antidepressants with anti-inflammatory properties [ 26 ]. Kubera et al [ 27 ] found that antidepressants increase IL-6 in animal models and in humans with depression.…”

Immunogenicity of decellularized extracellular matrix scaffolds: a bottleneck in tissue engineering and regenerative medicine

“…After recognition by PRRs, DAMPs promote the transcription of genes contributing to the inflammation process. 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]. The increase in the production of pro-inflammatory cytokines also induces a shift in the polarization of macrophages as the critical determinant of grafts' long-term prognosis toward the M1 phenotype [41,42].…”

Interplay between Serotonin, Immune Response, and Intestinal Dysbiosis in Inflammatory Bowel Disease

“…In both UC and CD, there is also involvement of the CNS, specifically leading to psychological or psychiatric manifestations [ 119 ]. It has been observed that between 15% and 25% of patients with IBD developed depression, while 30% presented with anxiety [ 120 ]. Furthermore, it may be accompanied by sleep difficulties and fatigue [ 121 ].…”