Host Intestinal Signal-Promoted Biofilm Dispersal Induces Vibrio cholerae Colonization

Abstract

Vibrio choleraecauses human infection through ingestion of contaminated food and water, leading to the devastating diarrheal disease cholera.V. choleraeforms matrix-encased aggregates, known as biofilms, in the native aquatic environment. While the formation ofV. choleraebiofilms has been well studied, little is known about the dispersal from biofilms, particularly upon entry into the host. In this study, we found that the exposure of mature biofilms to physiologic levels of the bile salt taurocholate, a host signal for the virulence gene induction ofV. cholerae, induces an increase in the number of detached cells with a concomitant decrease in biofilm mass. Scanning electron microscopy micrographs of biofilms exposed to taurocholate revealed an altered, perhaps degraded, appearance of the biofilm matrix. The inhibition of protein synthesis did not alter rates of detachment, suggesting thatV. choleraeundergoes a passive dispersal. Cell-free media from taurocholate-exposed biofilms contains a larger amount of free polysaccharide, suggesting an abiotic degradation of biofilm matrix by taurocholate. Furthermore, we found thatV. choleraeis only able to induce virulence in response to taurocholate after exit from the biofilm. Thus, we propose a model in whichV. choleraeingested as a biofilm has coopted the host-derived bile salt signal to detach from the biofilm and go on to activate virulence.