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In recent years, impressive advances in the knowledge about a vast number of microbes living in the human body and interactions between the microbiota and the human body have been observed. All micro-organisms that live in the human body consist of around 10 ^ 14 cells. The number of microbial cells colonizing the human body is ten times higher than the number of its own cells and the weight of all micro-organisms is about 2-2.5 kg. The number of bacterial genes is 50-100 times greater than the number of genes in the human body. Nowadays, the human microbiota is often regarded as a “newly discovered organ” or even as a “supergenome”. The results of many studies have revealed that disruption of the bowel microecosystem may affect the development of irritable bowel syndrome (IBS) symptoms. Therefore, manipulation of the gut microflora was hoped to be a new tool in the treatment of this disease. Various methods (probiotics, prebiotics, antibiotic therapy, transplantation of faecal flora) have been used to modify the intestinal microbiota by supporting the expansion of bacteria considered beneficial and reducing the number of those regarded as harmful, thus alleviating the IBS symptoms. There is much evidence in the literature to suggest that the intestinal microbiota and the gut-intestinal axis are important factors in the pathogenesis of IBS. Moreover, the literature findings have demonstrated beneficial effects of modifying the intestinal flora composition in alleviating IBS symptoms. Although the pathophysiology of IBS and the role of the intestinal microflora and gut-intestinal axis in it are well known, many issues are still to be elucidated. Further research into the bacteria identified in stool and colon mucosa of healthy individuals should provide more information on restoration of intestinal homeostasis in IBS patients.

Inflammatory bowel disease (IBD) comprises ulcerative colitis (UC) and Crohn disease (CD). Similar symptoms, but different treatment procedures for both diseases require precise diagnosis. MicroRNAs (miRNAs) are major posttranscriptional players that regulate the expression of genes during the inflammation and thus could be appropriate biomarkers for differentiation between UC and CD. For this purpose, we analyzed the expression of miR-21-3p, miR-31-3p, miR-125b-1-3p, miR-146a-3p, miR-155-5p, and E-cadherin (CDH1) genes associated with IBD, in 67 tissue samples: 28 inflamed mucosa samples (n=16 UC, n=12 CD), 28 adjacent normal colonic mucosa (n=16 UC, n=12 CD), and 11 normal mucosa from healthy patients using reverse transcription real-time RT-PCR. We found all analyzed miRNAs were significantly overexpressed in UC tissue as compared to adjacent normal tissue of patients with UC, as well as to normal mucosa from healthy controls. Four miRNAs (except miR-125b-1-3p) were significantly upregulated in CD lesions as compared to adjacent normal tissue of patients with CD, and four miRNAs, except miR-146a-3p, were significantly higher in CD samples compared to normal mucosa from healthy individuals. In the CD group, we found an inverse correlation between miR-155-5p or miR-146a-3p expressions and CDH1expression in inflamed mucosa. This type of correlation was also detected for miR-213p in adjacent normal tissue and CDH1 in inflamed mucosa, as well as between miR-155-5p and CDH1 in adjacent normal tissue. Elevated miRNA expression is characteristic for IBD-mediated inflammation process and inversely correlated with CDH1 gene expression, which suggest involvement of epithelial to mesenchymal transition (EMT) in IBD development.

Summary Background This study sought to define the mechanism by which PPAR-γ ligands affect the course of experimentally induced colitis in rats. Material/Methods Inflammation was induced in Wistar rats by a single rectal administration of 2,4,6,-trinitrobenzene sulfonic acid (TNBS). The antagonist of PPARγ antagonist, bisphenol A diglycidyl ether (BADGE), was administrated intraperitoneally 120 mg/kg 4 times every other day. Rosiglitazone 8 mg/kg was administrated by gastric tube 4 times. Body weight was measured daily. After killing, the large intestinal tissue was weighed and collected for histopathologic and immunoenzymatic tests. Levels of IL-6, IL-10, and myeloperoxidase (MPO) were determined in serum and in intestinal homogenates. Results Rats receiving rosiglitazone had higher body weight, whereas large intestine weight/length ratio was lower; histology showed fewer inflammatory markers. Rats receiving TNBS and TNBS along with BADGE had more intensive inflammatory changes. Rosiglitazone alone decreased expression of IL-6; used with TNBS it decreased expression of MPO in intestinal tissue, yet did not increase the expression of IL-10. Decreased levels of MPO indicate reduced neutrophil-dependent immune response. The antagonist of PPAR-γ increased IL-6 in serum and decreased IL-10 in intestinal homogenates. Bisphenol A diglycidyl ether administrated to healthy animals increases serum IL-6 levels. Conclusions Rosiglitazone inhibits experimental inflammation; administration of its selective antagonist abolishes this protective influence. Rosiglitazone inhibits expression of proinflammatory IL-6 and does not affect IL-10. Agonists of PPARs-γ are possibilities for inflammatory bowel disease prevention. Exogenous substances blocking PPARs-γ may contribute to development or relapse of nonspecific inflammatory bowel diseases.