Characterisation of Host Gut-Microbiota Interaction in the Drosophila Model of Dextran Sulfate Sodium (DSS)-induced Colitis

Inflammatory bowel diseases appear as highly heterogeneous, less-manageable chronic diseases. There is a remarkable progress in developing experimental colitis models which is a prerequisite to enrich the pharmacological armamentarium with new drugs. Yet, dextrans sulfate sodium (DSS)-induced colitis is widely implemented in different vertebrate model organisms. Although DSS was used to study multiple evolutionary-conserved pathways of cell injury in the Drosophila gut, a deep and integrative phenotyping of the DSS-induced injury is lacking. Here, a translational Drosophila model of DSS-induced colitis was established followed by a systematic characterization of disease endpoints and interrogation of host-microbiota interactions. Disease endpoints represent intestinal and extra-intestinal manifestations of the DSS-induced colitis. Significant reduction in the total activity, the food consumption, the excreta egestion and the body weight as well as marked gut leakiness and epithelial dysplasia were the main characteristic core phenotyping parameters (CPPs). Additionally, a significant increase of plasmatocytes (functional homolog of macrophages) recruitment to the injured gut was observed in response to DSS treatment.Given that microbiota plays a cardinal role in modulating gut physiology, targeted metagnomics was conducted on the established Drosophila DSS-colitis model. Results underscored that 16S rRNA profiling of tissue-associated microbiota was superior to that of the fecal microbiota community. Moreover, profiling midgut microbiome after DSS treatment identified a regionalized microbiota signature that was characterized by a significant reduction of alpha-diversity and blooming of Proteobacteria


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