To date, it is estimated that there are 2.9 million cases of cholera each year, resulting in 95,000 deaths. In an attempt to remedy this situation, the WHO has set an ambitious target: to eliminate cholera from high-risk areas by 2030. One of the reasons explaining the difficulty to eradicate this pathogen is that this bacterium is able to thrive in nutrient-poor environments, and particularly in phosphate-depleted areas.

While the vast majority of marine waters are limited by essential nutrients such as inorganic phosphate, coastal areas are subject to phosphate waves. In addition, global warming is expected to exacerbate nutrient deficiency in surface ocean. To survive in phosphate-limited environment, V. cholerae regulates genes belonging to the Pho regulon and remodels its membrane using the PhoBR two-component regulatory system. In the environment, bacteria are under constant predation pressure from heterotrophic protists such as Uronema marinum, a ciliate that graze on bacteria, thereby controlling their population. Previous studies have shown that V. cholerae is able to escape digestion by protists and that bacteria that have passed through these predators are more infectious to humans.

This study aims to explore the modification induced by phosphate depletion in V. cholerae membrane using ‘omics' approaches and how this affects its interaction with one of its main predators.

We have identified two new glycolipids, an amino acid-based lipid in addition to a modification of the LPS structure in V. cholerae membrane under phosphate-limited conditions. We have shown that V. cholerae grown in phosphate-deficient conditions is more captured and in greater quantities by the ciliate than those grown in a phosphate-rich medium. Our results suggest that the activation of PhoBR system may promote the concentration of V. cholerae in heterotrophic protists compartments, leading to the emergence of potential hyper-infectious outbreak.