Adherent-invasive E. coli in Crohn disease: bacterial “agent provocateur”
Warren Strober
Warren Strober
Published March 1, 2011; First published February 21, 2011
Citation Information: J Clin Invest. 2011;121(3):841-844. https://doi.org/10.1172/JCI46333.
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Commentary

Adherent-invasive E. coli in Crohn disease: bacterial “agent provocateur”

Abstract

The role of adherent-invasive E. coli (AIEC) in Crohn disease (CD) has been in debate for decades. AIEC bacteria are found in the small intestine of patients with chronic CD, but it has remained unclear whether this infection is causal or secondary to underlying immune deficiencies in CD patients. In this issue of the JCI, Chassaing and colleagues demonstrate that AIEC bacteria express an adherence factor called long polar fimbriae (LPF) that aids in the binding of these bacteria to M cells overlying Peyer’s patches and subsequent entry into lymphoid tissue. These findings provide a mechanism of AIEC penetration but do not prove that AIEC is causing a primary infection in the Peyer’s patches that is necessary for the initiation or persistence of CD inflammation.

Authors

Warren Strober

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Figure 1

Proposed role of AIEC in the pathogenesis of CD.

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Proposed role of AIEC in the pathogenesis of CD. Left: CD is initiated b...
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.