During an infection, bacteria such as Pseudomonas aeruginosa use a cell-to-cell signalling system called quorum sensing to communicate and modify their behaviour as a collective population. Quorum sensing is mediated by diffusible chemicals released by bacteria and is required for efficient colonisation and infection in the body. Interfering with quorum sensing is seen as an attractive new treatment option to combat resistance to antibiotics, which is an increasingly important global health issue.
It is known that the body is also able to sense the bacterial chemical signals and uses these to adjust how it fights back against the infection. However, the mechanism for detecting bacterial quorum sensing by the body is not understood. Pedro Moura Alves has previously shown that the Aryl hydrocarbon receptor (AhR), a ligand-dependent transcription factor that influences the immune response, can bind bacterial phenazines, which are downstream products of quorum sensing (Nature 2014). In this publication in Science, Pedro Moura Alves and Stefan Kaufmann (Max Planck Institute for Infection Biology, Berlin) show that the AhR can also detect a range of quorum sensing molecules. This allows the body to respond appropriately to the stage of bacterial infection and not expend unnecessary energy on immune responses if bacterial levels are below the threshold of causing harm. Further, with a greater understanding of the AhR-quorum sensing cross-talk, this pathway could be exploited as a new host-directed therapeutic strategy against P. aeruginosa, a notable pathogen in cystic fibrosis patients.