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Pseudomonas aeruginosa  controls production of its multiple virulence factors and biofilm development via the quorum sensing (QS) system. QS signals also interact with and affect the behavior of eukaryotic cells. Host water homeostasis and aquaporins (AQP) are essential during pathological conditions since they interfere with the cell cytoskeleton and signaling, and hereby affect cell morphology and functions. We investigated the contribution of  P. aeruginosa  QS genes  lasI/rhlI  to phagocytosis, cell morphology, AQP9 expression, and distribution in human macrophages, using immunoblotting, confocal, and nanoscale imaging. Wild type  P. aeruginosa  with a functional QS system was a more attractive prey for macrophages than the  lasI/rhlI  mutant lacking the production of QS molecules, 3O-C 12 -HSL, and C 4 -HSL, and associated virulence factors. The  P. aeruginosa  infections resulted in elevated AQP9 expression and relocalization to the leading and trailing regions in macrophages, increased cell area and length; bacteria with a functional QS system  lasI/rhlI  achieved stronger responses. We present evidence for a new role of water fluxes via AQP9 during bacteria–macrophage interaction and for the QS system as an important stimulus in this process. These novel events in the interplay between  P. aeruginosa  and macrophages may influence on the outcome of infection, inflammation, and development of disease.

frontiers in microbiology

Pseudomonas aeruginosa lasI/rhlI quorum sensing genes promote phagocytosis and aquaporin 9 redistribution to the leading and trailing regions in macrophages