Fig. 7.

Model of bacillary dysentery. a In the absence of intracellular invasion (i.e. ΔT3SS mutant) of epithelial cells (green), S. flexneri (red) is present in the lumen, and red blood cells (tangerine) are confined to blood vessels (black line). Infected animals do not display any symptoms (no bloody diarrhea). b In the absence of cell-to-cell spread (i.e., ΔicsA mutant), S. flexneri grows as micro-colony in primarily infected cells, but does not get access to adjacent cells. Epithelial cell production of signaling molecules (not shown) and vascular lesions (doted black line) lead to the infiltration of immune cells (neutrophils, purple) and red blood cells, respectively. In the absence of cell-to-cell spread, infected epithelial cells may undergo cell death (pale green) and be extruded from the epithelium. Fenestration of the epithelial layer is minimal and animals do not display any symptoms (no bloody diarrhea). c Wild-type S. flexneri invades epithelial cells and spreads from cell to cell. Similar to b, intracellular invasion leads to immune cell infiltration and vascular lesions. In addition, cell-to-cell spread leads to massive epithelial cell fenestration, which correlates with bacillary dysentery symptoms (bloody diarrhea)