Abstract: Objective · To investigate the role and mechanism of glucagon-like peptide-1 receptor agonist (GLP-1RA) liraglutide in dextran sulfate sodium (DSS)-induced inflammatory bowel disease (IBD). Methods · The drinking water with DSS concentration of 3% was prepared by using DSS and sterile water, and the mice were free to drink for 7 days, to construct IBD model. The experimental mice were randomly divided into four groups with five mice in each group: the control group [drinking sterile water, intraperitoneal injection of phosphate buffered saline (PBS)], the liraglutide group (drinking sterile water, intraperitoneal injection of 0.6 mg/kg liraglutide), the model group (drinking DSS water solution, intraperitoneal injection of PBS) and the treatment group (drinking DSS water solution, intraperitoneal injection of 0.6 mg/kg liraglutide). During the experiment, the fecal morphology, body weight, and colon length were observed. And hematoxylin-eosin (H-E) staining was used to observe the degree of colitis in mice. Flow cytometry was used to detect the proportion of neutrophils and eosinophils, as well as the changes of the innate lymphoid cell (ILC) subsets and function in the colon. Results · Compared with the model group, the symptoms of loose stool and bloody stool were improved, and the shortened colon length was also improved (P=0.007) in the treatment group. H-E staining showed that the infiltration of inflammatory cells in the colon of the treatment group was significantly reduced. Flow cytometry analysis of the colonic lamina propria showed that the proportion of neutrophils in the colon of the treatment group was significantly reduced (P=0.004), and the proportion of eosinophils was also reduced (P=0.002); the proportion of ILC (ILC2) in group 2 decreased (P=0.032), but the proportion of ILC (ILC3) in group 3 increased (P=0.008); the cytokine interleukin-22 secreted by ILC3 was increased (P=0.008). Conclusion · Liraglutide may delay the development of IBD by affecting the proportion of ILC subsets and secretion function.

Key words: innate lymphoid cell (ILC), inflammatory bowel disease (IBD), glucagon-like peptide-1 receptor agonist (GLP-1RA), Liraglutide