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. Author manuscript; available in PMC: 2021 Dec 1.
Published in final edited form as: FASEB J. 2020 Oct 13;34(12):15922–15945. doi: 10.1096/fj.202001669R

FIGURE 10.

FIGURE 10

A proposed mechanism for the role of glucosylceramide in response to BFT. In a healthy colon, normal microbiota persists, cells maintain normal levels of glucosylceramide, and adherens junctions and tight junctions ensure cell-to-cell adhesion (A). When the host is colonized with ETBF, ETBF joins the microbiota and begins producing BFT, causing a decrease in CEC E-cadherin levels and an increase in glucosylceramide synthase expression (B). If glucosylceramide synthase is inhibited in a host colonized with ETBF, E-cadherin and tight junction protein 1 levels decrease, which leads to an increase in membrane permeability. Bacterial factors are able to pass through the membrane and interact with host immune cells in the lamina propria, triggering a Th17-driven pro-inflammatory immune response (C). Colonization with ETBF in the presence of CBE protects tight junctions and reduces membrane permeability (D)