Gastroenterology Research and Practice最新文献

Objective: NOTES gallbladder-preserving surgery (N-GPS) has been heralded as a new paradigm shift in minimally invasive surgery for chronic cholecystitis patients. The objective of this research was to evaluate the impact of N-GPS on the intestinal microbiota of patients. Methods: The study selected patients with benign gallbladder disease (BG group) within 1 week preoperative (BG_DPR stage) and followed up over 1 year postoperative (BG_YPO stage) and selected healthy controls (HC group) whose sex, age, and BMI index matched with patients at BG_YPO stage, too. Accordingly, stool samples from healthy controls and two stages of patients with benign gallbladder disease were collected; among them, the selected samples were sent for 16S rDNA sequencing with Illumina MiSeq platform, and then, the combined samples were sent for short-chain fatty acid (SCFA) analysis with GC-MS platform. Results: The result of alpha diversity of Shannon index showed that the difference among the two stages of BG group and HC group wasn't statistically significant, while the result of beta diversity based on the weighted UniFrac distance suggested that the structure of intestinal microbiota of BG group at YPO stage was closer to HC group. LEfSe analysis suggested that BG_YPO stage enriched genus, such as Enterocloster and Hungatella_A_128155, which improved bile acid metabolism. Compared with BG_DPR stage, BG_YPO stage and HC group enriched Faecalibacterium and Roseburia, but depleted Streptococcus, while fecal SCFA concentrations increased. Conclusion: Patients with benign gallbladder disease and chronic cholecystitis after N-GPS treatment for over 1 year improved gut microbial community structure. With the improving bile acid metabolism, SCFA-producing bacteria increased and pathobionts decreased, which helped the intestinal microbiota structure of BG group at YPO stage restore and close to HC group. Trial Registration: Chinese Clinical Trial Registry identifier: ChiCTR1900028267.

Background: Crohn's disease (CD) is a chronic intestinal inflammatory disease associated with genetic, environmental, and other unknown factors. Cluster of differentiation 36 (CD36) plays an important role in cancer, inflammation, and metabolic diseases. Although CD36 has recently been implicated in various diseases, its role in CD is still unclear. Methods: Blood samples were collected from patients with CD and healthy volunteers. Peripheral blood mononuclear cells (PBMCs) were isolated by density gradient centrifugation over Ficoll-Paque and labeled with monoclonal antibodies (CD14-APC and CD36-PE). Flow cytometer CytoFlex is used for analysis. Results: Twenty-nine patients with CD in remission, 42 patients with active CD, and 23 healthy volunteers were included in the study. Our results showed that the frequency of the CD14+CD36+ monocyte subset was increased in PBMCs from patients with active CD compared with patients in remission and healthy controls. However, CD36 on monocytes was lower in CD compared with the healthy controls. CD36 expression was decreased in patients with active CD compared with that of patients with CD in remission and healthy control subjects, but no difference was found between patients with CD in remission and healthy controls. Interestingly, we found negative correlations of CD36 with HBI, SES-CD, C-reactive protein, and neutrophil-to-lymphocyte ratio. Conclusions: These data indicate that monocyte CD36 associates with disease activity in CD and might be a potential biomarker for assessing the activity of CD.