Significant Succession of Intestinal Bacterial Community and Function During the Initial 72 Hours of Acute Pancreatitis in Rats

Abstract

Acute pancreatitis (AP) is followed by structural and functional changes in the intestine, resulting from microbiome dysbiosis. However, it remains unclear how gut microbiome changes within the initial 72h of onset. In this study, severe acute pancreatitis (SAP), mild acute pancreatitis (MAP), and sham operation (SO) were replicated in rat models. 16S ribosomal RNA gene sequencing was used to explore the gut bacteria community. The predicted Cluster of Orthologous Genes (COG) and Kyoto Encyclopedia of Genes and Genomes (KEGG) metabolic pathways were associated with the 16S rRNA profiles. Compared to the SO group, significant community succession was found during the initial 72h in AP group. At 72 h after AP induction, the Firmicutes/Bacteroidetes (F/B) ratios were significantly different, with the highest ratio in SAP group and the lowest in MAP group. Lactobacillus was the most abundant genus, but it nearly disappeared in SAP rats at 72 h. Clostridiaceae 1 and Clostridium sensu stricto 1 were significantly enriched in AP group. Bacteroidales S24-7 and Bacteroidales S24-7 group norank were enriched in MAP group, while Collinsella, Morganella, and Blautia were enriched in SAP group. Lactobacillus was significantly correlated with nine COGs. Nine COGs showed significant differences between AP group and SO group. Moreover, four COGs showed significant differences between the MAP and SAP groups. KEGG Level_3 pathways propanoate metabolism (Ko00640) in AP group was significantly higher than that in SO group. The aspartate‒ammonia ligase and four KEGG orthology terms of the AP group were lower than that in the SO group, respectively. All these results suggest that the intestinal bacterial community structure and function was changed during the initial 72h in AP rats. The intestinal F/B ratio and the relative abundance of Lactobacillus could be potential markers for early diagnosis of MAP and SAP. The genus Clostridium sensu stricto 1 was the most enriched genus in AP, and may be an important marker for AP.

Maternal obesity and resistance to breast cancer treatments among offspring: Link to gut dysbiosis

“…Bacteria genera that were present at a significantly higher abundance in the fecal samples in mice with cancer included Clostridium sensu stricto, Streptococcus and Turicibacter . Clostridium sensu stricto is highly elevated in pancreatitis 100 . Streptococcus is a well‐known pathogen and also a biomarker of several cancers 101 .…”

“…Clostridium sensu stricto is highly elevated in pancreatitis. 100 Streptococcus is a well‐known pathogen and also a biomarker of several cancers. 101 Turicibacter is increased when CD8+ T cells are ablated.…”

The Role of the Gut Microbiome in the Development of Acute Pancreatitis

“…Escherichia coli, Enterococcus and Enterobacteriaceae are documented as the main pathogens of secondary intestinal infections caused by AP [8]. It was reported that in AP, an imbalance exists in the flora ratio [9,10]. Intestinal aerobic bacteria showed a significant increase in their proportion, represented by Escherichia coli, Enterococcus, Enterobacter and Streptococcus, while anaerobic bacteria showed inhibition in growth, represented by Bifidobacterium, Bacteroidetes and Prevotella [6].…”

The role of gut microbiota in acute pancreatitis: new perspectives in pathogenesis and therapeutic approaches

“…In an animal experiment, Liu et al compared the compositional and functional changes of gut microbiota during different stages of AP, which revealed that Firmicutes/Bacteroidetes (F/B) ratios were significantly higher in severe AP group while lower in the mild AP group compared with control group at 72 hours after AP induction. [22] Zhu et al demonstrated that compared to mild and moderately severe AP, some specific microbiota of severe AP including Acinetobacter, Geobacillus , and Stenotrophomonas exhibited positive correlation with inflammatory cytokines (eg, TNF-α and IL-1β) as well as gut barrier injury indexes (eg, D-lactate and diamine oxidase). [12] Chen et al examined the classification of microbial community in ANP rat model and found the relative higher abundance of Escherichia–Shigella and Phascolarctobacterium in fecal samples from ANP group compared with the control group, and reductions in Paneth cell-derived antimicrobial peptides due to intestinal flora disorder may contribute to the development of intestinal barrier dysfunction in ANP.…”