FIG 7.

Structural and functional brush border lesions caused by diarrhea-associated Afa/Dr DAEC in enterocyte-like cells. The drawing on the left summarizes the observed cellular events. Afa/Dr DAEC interact with the brush border-associated hDAF and hCEACAM1, hCEA, and hCEACAM6 receptors (1). In turn, hDAF-associated signaling pathways, including protein tyrosine kinase(s), phospholipase Cγ, phosphatidylinositol 3-kinase, protein kinase C, and Ca²⁺, are activated (2). Loss of the brush border results in the disassembly of the microvillus cytoskeleton and induces defective expression of functional proteins, such as SI, DPP IV, SGLT1, and GLUT5 (3). (A and B) Low and high magnifications of transmission electron micrographs showing the well-ordered brush border microvilli of uninfected cells. (C to F) Low and high magnifications of transmission electron and scanning electron micrographs show the disappearance of the brush border at a late time postinfection. (Micrographs in panels A to F reprinted from reference 410.) (G and H) Micrographs show the observation by CLSM of immunofluorescence labeling of brush border-associated DPP IV (x-y section). (Reprinted from reference 412.)