Abstract
Diarrhoea is the second leading cause of death in children under the age of five. The bacterial species, Vibrio cholerae and enteropathogenic Escherichia coli (EPEC), are among the main pathogens that cause diarrhoeal diseases, which are associated with high mortality rates. These two pathogens have a common infection site—the small intestine. While it is known that both pathogens utilize quorum sensing (QS) to determine their population size, it is not yet clear whether potential bacterial competitors can also use this information. 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.
Highlights
Bacteria constantly monitor both their own population sizes and the composition of the different species in their surroundings via a mechanism known as quorum sensing (QS)
To reveal the cross-talk between V. cholerae and enteropathogenic E. coli (EPEC), both of which colonize the small intestine, we cultured wild-type (WT) EPEC in the presence of V. cholerae and examined the EPEC T3SS activity. To support both V. cholerae growth and the induction of EPEC T3SS, which requires growth conditions that simulate those in the human gastrointestinal tract[35], the bacterial strains were grown statically in a 1:1 (v/v) mixture of Dulbecco’s modified Eagle’s medium (DMEM) and Luria-Bertani (LB) medium in a tissue culture incubator
To determine whether the cholera autoinducer 1 (CAI-1) detection and response mechanism is found in other gastrointestinal bacterial pathogens, we examined the effect of CAI-1 on the T3SS activity of enterohaemorrhagic E. coli (EHEC) O157:H7 and Salmonella enterica serovar Typhimurium (SL1344)
Summary
Bacteria constantly monitor both their own population sizes and the composition of the different species in their surroundings via a mechanism known as quorum sensing (QS). The HapR expression level is raised, resulting in the repression of virulence and biofilm formation genes[8,11,13,18] This multi-factor coordination is critical to the ability of V. cholerae to colonize its host when the bacterial population density is low and to adapt bacteria for transmission once it becomes critically high. E. coli strains, including EPEC, lack the luxI gene and cannot synthesize AHLs21 They encode the SdiA protein, a LuxR homolog that recognizes a wide range of AHLs synthesized by other bacterial species and respond to it by activating acid resistance genes[22] and repressing virulence genes[23]
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