Shigella, the causative agent of bacillary dysentery, invades the colonic epithelium where it elicits an intense inflammation leading to tissular destruction. Key to bacterial virulence, type III effectors injected into host cells reorganize the actin cytoskeleton and regulate inflammatory responses. Much progress has been made recently in the characterization of these type III effectors. These findings have reshaped our view of Shigella invasion, suggesting a strategy to invade epithelial cells 'discretely' as an initial route of invasion, contrasting with the devastating inflammatory response associated with the disease's acute phase. The diverse roles of Shigella type III effectors highlight the complexity of an infection process where as little as a thousand bacteria are estimated sufficient to cause the disease in humans.
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