Abstract
The human intestinal microbiota plays a crucial role in protection against the infection of Vibrio cholerae, the etiological agent of the diarrheal disease cholera. A rare commensal bacterium, Paracoccus aminovorans, was previously identified to bloom in the intestines during V. cholerae infection in a cohort of patients exposed to the pathogen. However, how P. aminovorans interacts with V. cholerae has not been experimentally determined; moreover, whether any association between this bacterium alters the behaviors of V. cholerae to affect the disease outcome is also unclear. Here we show that P. aminovorans and V. cholerae together form dual-species biofilm structures with previously uncharacterized novel features. Using an infant mouse colonization model, we demonstrate that the presence of P. aminovorans within the murine small intestine enhances V. cholerae colonization in the same niche that is dependent on the production of the Vibrio exopolysaccharide (VPS), a major component of mature V. cholerae biofilm. Our study has identified a novel mechanism by which a microbiota species increases V. cholerae virulence, and we establish a plausible explanation for the increased abundance of specific microbiota species in individuals during V. cholerae infection.
Significance Statement While ample evidence suggests that the outcome of various enteric infections can be affected by the intestinal microbiota, how specific gut microbes change the behaviors of a pathogen is unclear. Here we characterize the interaction between Vibrio cholerae and a rare gut microbe, Paracoccus aminovorans, that is known to bloom in the intestines during active V. cholerae infection. These two bacteria form a dual-species biofilm structure and increases the host colonization efficiency of V. cholerae. To our knowledge, no prior study has demonstrated that an individual microbe increases V. cholerae virulence. Importantly, our study illustrates a novel mechanism of gut microbe-pathogen interaction that has the potential to alter the disease outcome.
Competing Interest Statement
The authors have declared no competing interest.
Footnotes
Competing Interest Statement: No competing interests.
