Background Helicobacter pylori (H. pylori) infection is associated with remodeling of gut microbiota. Many studies have found H. pylori infection and eradication therapy can alter the gut microbiota. However, few studies explored the impact of eradication therapy containing minocycline and metronidazole on gut microbiota. Aim The objective of the present study was to explore the changes of gut microbiota after H. pylori infection. Besides, learn more about the dynamic changes of gut microbiota during different stages of eradication treatment containing minocycline, metronidazole, bismuth agents and proton pump inhibitors. Methods Sixty stool samples from the patients with H. pylori infection before eradication, 14 and 42 days after eradication, and ten stool samples from non-infected individuals were collected. Subsequently, we performed 16S rRNA gene amplicon sequencing to analyze these samples, and the results were evaluated by using alpha diversity, beta diversity and microbial composition analyses. Phylogenetic Investigation of Communities by Reconstruction of Unobserved States was also used to predict the metabolic pathways according to the Kyoto Encyclopedia of Genes and Genomes database. Results The alpha and beta diversity of the microbiota changed significantly in H. pylori infected individuals, but returned to baseline 42 days after eradication therapy. At the genus level, the abundances of Bacteroidetes, [Ruminococcus]_gnavus_group, Ruminococcaceae_Incertae_Sedis, Tuzzrealla, Butyricicoccus were significantly lower in the H. pylori infected group. Bacterial abundance was also dynamically changing during eradication treatment. In addition, PICRUST analysis found the levels of uronic acid metabolism, uncharacterized transport system, and biosynthesis of unsaturated fatty acids were higher in H. pylori infected individuals than in the non-infected group. Conclusions Intestinal microbiota diversity, composition, functional predictions altered significantly after H. pylori infection, and gradually returned to healthy control levels after the application of eradication therapy containing minocycline and metronidazole in one month and a half.

Objective The small intestinal bacterial overgrowth (SIBO) in acute pancreatitis correlates with the severity of the disease. However, corresponding studies on the microbial composition of the duodenal mucosa of patients are uncommon. Methods Duodenal mucosal biopsies were collected by gastroscopy from 16 patients with mild acute pancreatitis (the Ap group) and 16 healthy individuals (the control group) and subjected to histological studies as well as bacterial 16S rRNA gene sequencing. Caerulein and l -arginine were used to induce mild acute pancreatitis (MAP) and severe acute pancreatitis (SAP) in mice, respectively, and their pancreas and duodenum were collected for histological studies. Results H&E analysis displayed no significant pathological damage in the descending duodenum of patients with acute pancreatitis compared with that of the controls. Immunofluorescence and Real-time PCR revealed that the expressions of tight junction proteins (TJPs) in duodenal mucosa were decreased in acute pancreatitis. The results of the alpha diversity analysis revealed no significant difference between the two groups, while LEfSe and the random forest revealed a few differences, indicating that the descending duodenum mucosal microbiota changed slightly in patients with mild acute pancreatitis. We observed the pathological changes and the expression of TJPs in the duodenum in the three groups of mice and found that SAP mice had more severe pathological damage in the duodenum. Furthermore, the expression of TJPs in the duodenum was lower in the MAP and SAP groups of mice compared to control mice, but it was similar in both groups. Conclusion Patients with mild acute pancreatitis had mild duodenal barrier dysfunction and slight changes in duodenal mucosal microbiota. Supplementary Information The online version contains supplementary material available at 10.1007/s10620-023-07948-8.

Background/Objectives: Gut microbiota dysbiosis is a complication of acute pancreatitis (AP). However, the composition of the pancreatic and ileal microbiota and their relationship during acute pancreatitis remain unknown. Methods: AP was induced in mice using three modeling methods, Caerulein (CAE), Caerulein+lipopolysaccharide (CAE+LPS) and L-arginine (ARG). Pancreas and ileum were collected for histological study and bacterial 16S rRNA gene sequencing to investigate the changes in the pancreatic and ileal flora under different inductions and their relationships. Blood samples were tested for amylase, lipase, and inflammatory markers, and histological investigations were done to assess pancreatic and ileal pathological damage. Results: All three modeling techniques led to inflammation and AP and ileal damage. Rarefaction and Shannon indices revealed that the pancreas and ileum of AP mice had higher levels of microbial diversity. Principal coordinate analysis (PCoA) and non-metric multidimensional scaling (NMDS) analysis showed microbial structural segregation in both the AP and control groups in the pancreas and ileum. In the three AP groups, there was microbial structural segregation between the ARG and the two CAE groups (CAE, CAE+LPS). Taxonomic analysis at the genus level showed a significant increase in the relative abundance of Muribaculaceae and a decrease in the relative abundance of Dietzia in the pancreas and ileum of AP mice. The same finding was found for linear discriminant analysis of effect size (LEfSe) at the operational taxonomic unit (OTU) level. In addition, the pancreas and ileum of both CAE groups were enriched with Roseburia, whereas the pancreas of the ARG group was enriched with Escherichia-Shigella. The abundance of Muribaculaceae and Dietzia in the pancreas is associated with that in the ileum, according to Spearman correlation analysis of the pancreatic and ileal microbiota. Conclusions: These results showed that when AP was induced, caerulein and L-arginine differentially affected the pancreatic and ileal microbiota.