The role of Vibrio Cholerae autoinducer-1 (CAI-1) in Enteropathogenic E. coli virulence

Diarrhea is the second leading cause of mortality of children under the age of 5 in developing countries according to the World Health Organization. Enteropathogenic E. coli (EPEC) and Vibrio cholerae are two main pathogens that cause diarrheal diseases and have a common infection site, the small intestine. EPEC infects intestinal cells by a specialized transport complex, called type III secretion system (T3SS), which is composed of approximately 20 different proteins. The T3SS resemble a nano syringe, which extends from the bacterial membrane to the plasma membrane of the host cell and injects virulence effector proteins into the host cells cytoplasm. Generally, bacteria rely on a variety of mechanisms in response to changing environmental conditions. One of such mechanism is Quorum Sensing (QS), which is known to be used by EPEC and V. cholerae to sense their population size. In this study, we examined the ability of EPEC to determine V. cholerae population sizes and to modulate its own virulence mechanisms accordingly. We found that EPEC virulence is enhanced in response to elevated concentrations of cholera autoinducer-1 (CAI-1), even though neither a CAI-1 synthase nor CAI-1 receptors have been reported in E. coli. This CAI-1 sensing and virulence upregulation response may facilitate the ability of EPEC to coordinate successful colonization of a host co-infected with V. cholerae. To the best of our knowledge, this is the first observed example of ‘eavesdropping’ between two bacterial pathogens that is based on interspecies sensing of a QS molecule.