Although the initial phases of intestinal infection with
Vibrio cholerae
have been intensively scrutinized, the later stages of infection, which are characterized by mass detachment of bacteria from epithelial surfaces and movement into the intestinal lumen, have been largely overlooked. Alex Nielsen and Nadia Dolganov, working in the Schoolnik laboratory, now redress this balance by providing insights into this luminal migration, which takes place about 12 hours after infection and which they call the 'mucosal escape response'. They reveal that this phenomenon is accompanied by the induction of a specific genetic programme in V. cholerae that activates a range of motility and chemotaxis genes.
The authors used a combination of confocal microscopy, expression profiling and mutant analysis to study the mucosal escape response in a rabbit model of V. cholerae infection, the ligated ileal-loop model. They first showed that 12 hours after inoculation in this model, at the time of bacterial detachment, V. cholerae replication slows to a rate similar to that of organisms entering stationary phasein culture. The stationary phase alternative sigma factor RpoS is required for the mucosal escape response, evidenced by the fact that an rpoS mutant strain did not detach from ileal-loop epithelial cells. HapR, an RpoS-controlled factor that downregulates virulence determinant expression and biofilm formation, is also required for this stage of cholera infection.
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