Giardia duodenalis genotype A and B are responsible for post infectious visceral hypersensitivity in an immunocompetent suckling rat model: Is commensal bacterial translocation one of the mechanisms leading to PI‐IBS?

Enteric pathogens such as Giardia duodenalis , common waterborne protozoan parasite, have been linked to Post‐infectious Irritable Bowel Syndrome (PI‐IBS) a functional intestinal disorder, in which visceral hypersensitivity is a key factor. We aimed to develop a model characterizing PI‐IBS triggered by Giardia infection and, reveal mechanisms responsible for the PI‐IBS‐like symptoms, such as the role of the commensal microbiota. Five day‐old Sprague‐Dawley rats gavaged with 10 4 trophozoites (genotypes A or B) were assessed for visceral hypersensitivity 50 days post‐infection (PI) via jejunal/rectal balloon distension. Changes in blood pressure were recorded as measurements of visceral hypersensitivity. Caco‐2 monolayers were used to assess if Giardia facilitates the translocation of a non‐invasive E. coli at various time points. On day 50 PI, jejunal and rectal hypersensitivity was observed with both genotypes. G. duodenalis also facilitated translocation of non‐invasive E. coli through Caco‐2 monolayers 3h PI. Hypersensitivity was detected in the jejunum, as well as in the rectum, a site beyond the infection area, indicating that the effect is not limited to the presence of the pathogen. Giardia facilitates the passage of non‐invasive bacteria through the intestinal epithelium, mechanism which could cause PI‐IBS. This study describe a new model for the study of protozoa‐induced PI‐IBS. fundings: NSERC Create, FFCR (France‐Canada Research Fund), CCFC