Dextran sodium sulfate-induced colitis-like gut permeability and dysbiosis in honeybees.

The gut microbiota has been linked to the pathophysiology of inflammatory bowel disease (IBD). Current animal models are limited in the generation of germ-free animals to evaluate the roles of gut bacteria in intestinal health. Here, we used the honeybee (Apis mellifera) as a model animal to develop colitis-like gut permeability induced by dextran sodium sulfate (DSS) treatment. We found that DSS could increase gut permeability and compromise the mucosal barrier in honeybees, resulting in decreased survival rates, midgut elongation, and intestinal edema. DSS treatment upregulated the expression of wnt-1 and rhomboid and downregulated the pathways of cytochrome P450 (CYP) and the peroxisome proliferator-activated receptor signaling. Moreover, DSS disrupted the structure and functional profiles of the gut microbiota. Our results showed that medications reduced mortality and moderated leaky gut syndrome in DSS-treated bees. Notably, 5-aminosalicylic acid (5-ASA) could attenuate gut permeability in honeybees through activating PPARγ signaling, which mimics the human. Honeybees offer a promising experimental model for investigating the etiology of intestinal diseases and disentangling the roles of gut symbionts in intestinal health.