Molecular Basis of the Intracellular Spreading of Shigella

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Abstract
Shigella causes bacillary dysentery, a disease provoking se- vere bloody and mucous diarrhea. When the pathogen reaches the colon, bacteria translocate through the epithelial barrier by way of the M cells that overlay the solitary lymphoid nodules (71, 72, 91). Once it reaches the underlying M cells, Shigella infects the resident macrophages and induces cell death. The infected macrophages release large amounts of interleukin-1, which finally leads to a strong inflammatory response (101). Meanwhile, a bacterium released from the macrophages enters enterocytes via the basolateral surface by directing membrane ruffling and macropinocytosis. The bacterium is surrounded by a phagocytic vacuole; however, it immediately disrupts the membrane to escape into the cytoplasm, where it can multiply and move by inducing actin polymerization at one pole of the bacterium, allowing intracellular spread within the cytoplasm as well as into adjacent epithelial cells (3, 44). In response to bacterial infection, epithelial cells are elicited to produce pro- inflammatory cytokines, further promoting local inflammation in the colon. Thus, the ability of Shigella spp. to infect host cells, including the continuous intra- and intercellular spread- ing, is essential for leading to bacillary dysentery.