J Clin Invest.
Proposed role of AIEC in the pathogenesis of CD.
Left: CD is initiated by a genetically determined (AIEC-independent) mucosal immune response to components of the resident gut microflora; this includes the production of proinflammatory cytokines such as IL-12p70 and IFN-γ. Middle: The inflammatory response leads to increased expression of an epithelial binding site, CEACAM6, on polarized epithelial cells and thus sets the stage for the selective proliferation of preexistent E. coli with an AIEC phenotype. Right: AIEC bacteria enter the Peyer’s patches via binding of LPF to GP2 on the surface of M cells overlying the patches; within the patches, they can exacerbate inflammation by inducing innate immune responses of patch macrophages; AIEC can also enter the lamina propria, probably via ulcerations resulting from the inflammation, and exacerbate inflammation at this site as well.