Dysentery bug Shigella flexneri spreads from cell to cell via cytoskeletal-created compartments
A driver in a traffic jam blasts an annoying catchy song. The next driver hears it, and whistles along. Then another hums it, and soon the whole street is a cacophony of unsynchronised earworms. The song might have been contained within the first car by a closed window, and that’s what a new molecule may do for dysentery-causing Shigella flexneri infections, which spread between cells lining the intestine's colon. The bacteria use a host cell’s internal skeleton to create protrusions towards neighbouring cells, which bud off as sac-like structures known as vacuoles to transmit the infection. A study identified a protein required for this conversion from protrusion to vacuole, and a molecule that inhibits it, thus preventing spread (pictured, red bacteria limited to isolated spots in an infected rabbit colon after treatment with the inhibitor). This could be a new route to treatment for a condition with no vaccine and increasing risk of drug resistance.
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