Dysbiosis promotes recurrence of adenomatous polyps in the distal colorectum

BACKGROUND Colorectal polyps,which are characterized by a high recurrence rate,represent preneoplastic conditions of the intestine.Due to unclear mechanisms of pathogenesis,first-line therapies for non-hereditary recurrent colorectal polyps are limited to endoscopic resection.Although recent studies suggest a mechanistic link between intestinal dysbiosis and polyps,the exact compositions and roles of bacteria in the mucosa around the lesions,rather than feces,remain unsettled.AIM To clarify the composition and diversity of bacteria in the mucosa surrounding or 10 cm distal to recurrent intestinal polyps.METHODS Mucosal samples were collected from four patients consistently with adenomatous polyps(Ade),seven consistently with non-Ade(Pol),ten with current Pol but previous Ade,and six healthy individuals,and bacterial patterns were evaluated by 16S rDNA sequencing.Linear discriminant analysis and Student’s t-tests were used to identify the genus-level bacteria differences between groups with different colorectal polyp phenotypes.Pearson’s correlation coefficients were used to evaluate the correlation between intestinal bacteria at the genus level and clinical indicators.RESULTS The results confirmed a decreased level of probiotics and an enrichment of pathogenic bacteria in patients with all types of polyps compared to healthy individuals.These changes were not restricted to the mucosa within 0.5 cm adjacent to the polyps,but also existed in histologically normal tissue 10 cm distal from the lesions.Significant differences in bacterial diversity were observed in the mucosa from individuals with normal conditions,Pol,and Ade.Increased abundance of Gram-negative bacteria,including Klebsiella,Plesiomonas,and Cronobacter,was observed in Pol group and Ade group,suggesting that resistance to antibiotics may be one risk factor for bacterium-related harmful environment.Meanwhile,age and gender were linked to bacteria changes,indicating the potential involvement of sex hormones.CONCLUSION These preliminary results support intestinal dysbiosis as an important risk factor for recurrent polyps,especially adenoma.Targeting specific pathogenic bacteria may attenuate the recurrence of polyps.

Prognostic value of Muc5AC in gastric cancer: A meta-analysis

AIM: To assess the correlation between decreased Muc5 AC expression and patients' survival and clinicopathological characteristics by conducting a metaanalysis.METHODS: Literature searches were performed in Pub Med and EMBASE,and 11 studies met our criteria. Summary hazard ratios or odds ratios(ORs) with 95% confidence intervals(CIs) were calculated to estimate the effect. For the pooled analysis of the correlation between decreased Muc5 AC expression and clinicopathological characteristics(tumour invasion depth,lymph node metastasis,tumour-node-metastasis stage,tumour size,venous invasion and lymphatic invasion),ORs and their variance were combined to estimate the effect. RESULTS: Eleven retrospective cohort studies comprising 2135 patients were included to assess the association between Muc5 AC expression and overall survival and/or clinicopathological characteristics. Decreased Muc5 AC expression was significantly correlated with poor overall survival of gastric cancer patients(pooled HR = 1.35,95%CI: 1.08-1.7). Moreover,decreased Muc5 AC expression was also significantly associated with tumour invasion depth(pooled OR =2.12,95%CI: 1.56-2.87) and lymph node metastasis(pooled OR = 1.56,95%CI: 1.00-2.44) in gastric cancer.CONCLUSION: Decreased Muc5 AC expression might be a poor prognostic predictor for gastric cancer.

Synthesis of Toll-like receptor 4 in Kupffer cells and its role in a lcohol-induced liver disease

s To observe the synthesis of Toll like receptor (TLR) 4 protein and its mRNA exp ression in Kupffer cells (KCs) and evaluate the role of TLR 4 in liver injury to rats through alcohol induced liver disease Methods Twenty eight Wistar rats were divided into two groups: ethanol fed (group E) a nd control (group C) Group E rats were given ethanol at a dose of 5-12 g·kg 1 ·d 1 , while group C received dextrose Animals from bot h groups were killed at 4 and 8 weeks The KCs were isolated and synthesis of T LR 4 protein was determined by laser scanning confocal microscopy TLR 4 mRNA e xpression in KCs was determined by reverse transcription polymerase chain reacti on (RT PCR) analysis The levels of endotoxin, tumor necrosis factor α (TN F α) and interleukin 6 (IL 6) in plasma were determined Changes in liver pathology were observed Results Laser scanning confocal microscopy showed that the intensity of fluorescence of TLR 4 protein in group E was stronger than group C Ethanol administration led to a significant increase in TLR 4 mRNA expression in group E compared with grou p C ( P <0 05) The concentrations of plasma endotoxin, TNF α and IL 6 were higher in group E than in group C ( P <0 05) Liver sections from rat s in group E demonstrated marked pathological changes Conclusion Ethanol administration can lead to the synthesis of TLR 4 protein and its gene e xpression in KCs, indicating that TLR 4 may play a major role in the development of alcohol induced liver injury

In vivo expression of lipopolysaccharide binding protein and its gene induced by endotoxin

Objective: To investigate the expression of lipopolysaccharide binding protein (LBP) and its gene in rats with endotoxemia and explore the role of LBP in the response of host to endotoxin. Methods: Thirty Wistar rats were divided randomly into five groups: the normal group and the endotoxemia groups (1, 3, 6, 12 hours after LPS injection, respectively). The level of plasma endotoxin was determined by the Limulus Amebocyte Lysate assay. The expression of LBP mRNA in hepatic tissue was examined by reverse transcription polymerase chain reaction (RT PCR). Plasma levels of LBP, tumor necrosis factor (TNF) α and interleukin (IL) 6 were measured by enzyme linked immunosorbent assay (ELISA). Morphologic changes of hepatic tissue were observed under transmission electron microscope. Results: The level of plasma endotoxin peaked at 1 h after LPS injection, then declined, but was still higher than that of the normal group at 12 h; intrahepatic expression of LBP mRNA and plasma LBP increased with time after LPS stimulation; TNF α and IL 6 in plasma increased with upregulation of LBP expression; there were significant differences between the normal group and endotoxemia groups (P< 0.05 ). Activation of Kupffer cells and injury of hepatocytes could be seen in rats with endotoxemia. Conclusions: LPS can upregulate the intrahepatic expression of LBP mRNA and increase the plasma LBP level. Under certain conditions, LBP may enhance the sensitivity of host to the toxic effects of LPS.