We tested the hypothesis that genetic polymorphisms and haplotypes of CRHR2 are associated with IBS pathophysiology and negative emotion in IBS patients.
We examined CRF2 gene and protein expression in the distal/sigmoid colonic mucosal biopsies from healthy subjects and patients with UC (active or disease in remission), human immunodeficiency virus (HIV) and functional bowel disease (FBD) by reverse transcription-polymerase chain reaction and immunofluorescence.
TC-IBS showed a pronounced depression phenotype with increased corticotropin-releasing hormone receptor (CRHR)1 and CRHR2 expression at the frontal cortex and increased serum ACTH concentration.
MiRNA-29a knockout resulted in overexpression of HTR7 and attenuated visceral hyperalgesia in WAS-induced IBS mice.HTR7 was a direct target of miRNA-29a.
In this mini review, we briefly summarize recent progress in intestinal fructose metabolism, regulation and function of ChREBP by fructose, and delineate the potential mechanisms by which excessive fructose consumption may lead to irritable bowel syndrome.[BMB Reports 2018; 51(9): 429-436].
We evaluated the effect of DIM on the intestinal permeability of human intestinal cell monolayers and the animal model <i>Caenorhabditis elegans,</i> which were treated with IL-1β and <i>Pseudomonas aeruginosa</i>, respectively, to mimic IBD conditions.
When comparing IBS subtypes, TNFα and IL-17 were significantly (P<0.05) higher, and IL-10 was significantly (P<0.05) lower in diarrhea predominant IBS (IBS-D) compared to HCs, whereas the inflammatory cytokine profile of other subtypes more closely resembled that of HCs.
Ten relevant genes were evaluated.SNPs rs4263839 and rs6478108 of TNFSF15 associated with an increased risk of IBS; IL6 rs1800795 increased the risk for Caucasian IBS patients which diagnosed by Rome III criteria; and IL23R rs11465804 increased the risk for IBS-C patients.
Correlation analysis revealed that in patients with IBS-D (P < .001) and PI-IBS (P < .05), the levels of PRDX1 and TNF-α in sera had a significant positive correlation with IBS-SSS.
The secretion of proinflammatory cytokines (IL-1β and IL-6) in mice with IBS was significantly increased compared with that of the control group, which suggested that the intestinal mucosa in mice with IBS was in a low-grade inflammatory state.
Here we aimed to assess the anti-inflammatory effect and the mechanism of action of sialorphin, the natural blocker of the endogenous opioid peptide-degrading enzymes neprilysin [NEP] and aminopeptidase N [APN], in mouse models of IBD and the changes in the expression of these enzymes in IBD patients.
Most appreciated were the topics brain imaging of gut activity, the role of the gut microbiota, the pharmacology of gut functions, the IBS-IBD interrelation, the new Rome IV criteria, the role of gas, and the placebo response in functional disorders.
Subsequently, expression of tumor necrosis factor-α (TNF-α), interleukin-2 (IL-2), and IL-6 were detected to further determine the effects of miR-181c-5p and IL1A on inflammation in IBS. miR-181c-5p and IL1A might be involved in IBS. miR-181c-5p was found to be decreased while IL1A was increased in IBS rats.
Moreover, IL-1beta mRNA expression had increased in biopsies taken from INF-IBS patients at three months after the acute infection but no consistent change was observed in INF-CON patients.
IBS-D and PI-IBS patients are associated with TNFSF15 and TNFα genetic polymorphisms which also predispose to Crohn's disease suggesting possible common underlying pathogenesis.