Ahn SB, et al. Gut Liver. 2012 Jan;6(1):64-70. http://dx.doi.org/10.5009/gnl.2012.6.1.64

A close relationship between inflammation and colon cancer has been widely accepted, and interleukin (IL)-17A plays an important role in controlling colonic inflammation. However, the role of IL-17A has not yet been validated in colitis-associated cancer (CAC). This study aims to identify the effects of IL-17A in tumorigenesis utilizing IL-17A-deficient mice in an experimental CAC model. CAC was induced in both the IL-17A-deficient and the C57BL/6 (wild-type, WT) mice by injection of 12.5 mg/kg azoxymethane followed by three rounds of 1.7% dextran sodium sulfate exposure to elicit colitis. On day 63 after the start of the study, mice were sacrificed. Colonic inflammation, proliferation and tumorigenesis were evaluated. Tumor numbers per mouse (1.43 versus 5.80; P = 0.02) and mean tumor size (1.17 versus 3.58 mm; P = 0.01) were significantly decreased in IL-17A-deficient mice compared with WT mice. Furthermore, the inflammation and the proliferation scores of IL-17A-deficient mice were significantly lower than WT mice. In the analysis of inflammatory mediators, IL-6, interferon-γ, tumor necrosis factor-α and IL-17A were markedly decreased in IL-17A-deficient mice compared with WT mice. In the western blot analysis, p-STAT3, cyclin D1, cyclin-dependent kinase 2, cyclin E, Glycogen synthase kinase 3-β and p-Akt were downregulated in IL-17A-deficient mice. Immunohistochemical staining with p-STAT3, Ki-67 and β-catenin revealed lower number of stained cells in IL-17A-deficient mice compared with WT mice. IL-17A ablation significantly decreases CAC tumorigenesis and thus may play an important role associated with chronic colitis.

Background Inadequate bowel preparation is important because it can result in missed lesions, cancelled procedures, increased procedural time, and a potential increase in complication rates. This prospective study was designed to look at the quality of colon preparation using polyethylene glycol solution and evaluate potential associations between specific patient characteristics and inadequate bowel preparation. Methods A total of 362 patients who were compliant with preparation instructions were enrolled. All colonoscopic examinations were performed by an experienced endoscopist and the quality of the preparation was graded by the endoscopist (excellent to poor). Patient demographic and medical history information was gathered before the procedure. Possible predictors of inadequate colonic preparation were analyzed using univariate statistics and multivariate logistic regression models. Results An inadequate bowel preparation was reported in 28.2% of observed colonoscopies. In multivariate regression analysis, age greater than 60 years [odds ratio (OR) 2.8, 95% confidence interval (CI) 1.04-7.4], a history of diabetes (OR 8.6, 95% CI 6.3-19.4), a history of appendectomy (OR 4.6, 95% CI 2.0-10.5), a history of colorectal resection (OR 7.5, 95% CI 3.4-17.6), and a history of hysterectomy (OR 3.4, 95% CI 1.1-10.4) were independent predictors of an inadequate colon preparation. Conclusions This prospective study identified several factors that may predict inadequate polyethylene glycol preparation independent of compliance with preparation instructions and procedure starting time. This result may help to identify patients at an increased risk for inadequate bowel preparation for whom alternative preparation protocols would be beneficial.

In addition to genetic and epigenetic factors, various environmental factors, including diet, play important roles in the development of colorectal cancer (CRC). Recently, there is increasing interest in the intestinal microbiota as an environmental risk factor for CRC, because diet also influences the composition of the intestinal microbiota. The human intestinal microbiota comprises about 100 trillion microbes. This microbiome thrives on undigested dietary residues in the intestinal lumen and produces various metabolites. It is well known that the dietary risk factors for CRC are mediated by dysbiosis of the intestinal microbiota and their metabolites. In this review, we describe the bacterial taxa associated with CRC, including Fusobacterium nucleatum, enterotoxigenic Bacteroides fragilis, Escherichia coli, and butyrate-producing bacteria. We also discuss the host-diet interaction in colorectal carcinogenesis.

Background: Despite recent advances in studies on the gastric microbiome, the role of the non‐Helicobacter pylori gastric microbiome in gastric carcinogenesis remains unclear. We evaluated the characteristics of the gastric microbiome and metagenomic functions in patients with IM.Methods: Participants were classified into six groups according to disease status (chronic superficial gastritis [CSG], intestinal metaplasia [IM], and cancer) and H. pylori‐ infection status (H. pylori‐positive and H. pylori‐negative). The gastric microbiome was analyzed in mucosal tissues at the gastric antrum by 16S rRNA gene sequencing. Moreover, we assessed the metagenome including the type IV secretion system (T4SS) gene, as T4SS proteins are essential for transferring CagA from H. pylori- into the human gastric epithelium.Results: Among the 138 included patients, 48, 9, 23, 14, 12, and 32 were classified into the H. pylori‐negative CSG, H. pylori‐negative IM, H. pylori‐negative cancer, H. pylori‐positive CSG, H. pylori‐positive IM, and H. pylori‐positive cancer groups, respectively. Cyanobacteria were predominant in the H. pylori‐negative CSG group compared to in the H. pylori‐negative IM and H. pylori‐negative cancer groups (H. pylori‐negative CSG vs H. pylori‐negative IM vs H. pylori‐negative cancer: 14.0% vs 4.2% vs 0.04%, P < 0.001). In contrast, Rhizobiales were commonly observed in the H. pylori‐negative IM group (H. pylori‐negative CSG vs H. pylori‐negative IM vs H. pylori‐negative cancer: 1.9% vs 15.4% vs 2.8%, P < 0.001). The relative abundance of Rhizobiales increased as H. pylori‐infected stomachs progressed from gastritis to IM. In the H. pylori‐negative IM group, genes encoding T4SS were prevalent among the metagenome. Additionally, after H. pylori- eradication therapy, the gastric microbiome was similar to the microbiome observed after spontaneous clearance of H. pylori-.Conclusions: The relative abundance of Rhizobiales was higher in patients with H. pylori‐negative IM than in those with H. pylori‐negative CSG or cancer. Additionally, T4SS genes were highly observed in the metagenome of patients with IM. Highly abundant T4SS proteins in these patients may promote gastric carcinogenesis.