Exploring the effect of Clostridium butyricum on lung injury associated with acute pancreatitis in mice by combined 16S rRNA and metabolomics analysis

Objectives

Acute lung injury is a critical complication of severe acute pancreatitis (SAP). The gut microbiota and its metabolites play an important role in SAP development and may provide new targets for AP-associated lung injury. Based on the ability to reverse AP injury, we proposed that Clostridium butyricum may reduce the potential for AP-associated lung injury by modulating with intestinal microbiota and related metabolic pathways.

Methods

An AP disease model was established in mice and treated with C. butyricum. The structure and composition of the intestinal microbiota in mouse feces were analyzed by 16 S rRNA gene sequencing. Non-targeted metabolite analysis was used to quantify the microbiota derivatives. The histopathology of mouse pancreas and lung tissues was examined using hematoxylin–eosin staining. Pancreatic and lung tissues from mice were stained with immunohistochemistry and protein immunoblotting to detect inflammatory factors IL-6, IL-1β, and MCP-1.

Results

C. butyricum ameliorated the dysregulation of microbiota diversity in a model of AP combined with lung injury and affected fatty acid metabolism by lowering triglyceride levels, which were closely related to the alteration in the relative abundance of Erysipelatoclostridium and Akkermansia. In addition, C. butyricum treatment attenuated pathological damage in the pancreatic and lung tissues and significantly suppressed the expression of inflammatory factors in mice.

Conclusions

C. butyricum may alleviate lung injury associated with AP by interfering with the relevant intestinal microbiota and modulating relevant metabolic pathways.