Transfer of CD11c+ lamina propria mononuclear phagocytes from post-infectious irritable bowel syndrome causes mucosal barrier dysfunction and visceral hypersensitivity in recipient mice

The role of low-grade inflammation in the development of post-infectious irritable bowel syndrome (PI-IBS) has attracted increasing attention. Abnormal CD11c(+) mononuclear phagocytes, such as dendritic cells (DCs), macrophages, and monocytes, are involved in the disruption of immune tolerance in organisms, which can lead to the development of chronic inflammatory diseases. The present study tested the hypothesis that CD11c(+) lamina propria mononuclear phagocytes (CD11c(+) LPMPs) contribute to increased mucosal permeability and visceral hypersensitivity in a PI-IBS mouse model. CD11c(+) LPMPs were isolated and purified via the digestion of intestinal tissues and magnetic-activated cell sorting. We detected increased mucosal permeability, visceral hypersensitivity and intestinal inflammation during both the acute and chronic stages of Trichinella infection. Following the transfer of CD11c(+) LPMPs from PI-IBS mice into normal mice, low-grade inflammation was detected, as demonstrated by increased IL-4 expression in the ileum, as well as enhanced mucosal permeability, as indicated by decreased transepithelial electrical resistance and the presence of ultrastructural alterations. More importantly, the mice that underwent adoptive transfer of CD11c(+) LPMPs from the PI-IBS mice also exhibited increased abdominal withdrawal reflex scores and a decreased threshold. Our data demonstrated that the CD11c(+) LPMPs from this PI-IBS mouse model were not only able to transfer enteric inflammation to the normal mice but also caused abnormal intestinal function, characterized by epithelial barrier disruption and visceral hyperalgesia.