INA – SOURCES
One bacterium does not an infection cause; the microbes work as a team. Some species send and receive molecular signals so they can keep tabs on how many fellows surround them, a process known as quorum sensing. Virulence kicks into high gear when this signalling indicates that the bacterial population reaches a certain density threshold—the requisite quorum.
One species that relies on quorum sensing is P. aeruginosa, a nasty pathogen that infects and causes disease in plants, animals and, when an opportunity presents itself, in humans. It is a leading cause of morbidity and mortality in burn victims, people with cystic fibrosis, and people who are immune compromised, like AIDS patients. It is also a major contributor to nosocomial infections (infections that originate in hospitals). Obviously, it is resistant to multiple classes of antibiotics.
AhR is a protein found on the exterior of human cells that senses outside molecules. When activated by one of these molecules, it activates target genes. It was initially identified as the receptor that mediates the toxic effects of synthetic compounds like dioxins and related industrial pollutants.
But in 2014 it was found to also recognize quorum-sensing signals and destroy them. In this case it doesn’t mediate toxicity but, instead, marshals an immune response to bacterial infection.
Now, additional work has shown that AhR can not only recognize quorum sensing signals, it also monitors their levels to tailor the immune response to the specific stages of infection. Some quorum-sensing signals activate AhR, while others repress it, allowing the immune response to be adjusted based on what the bacteria are up to.
That's valuable, as immune responses can be as damaging to the host as the infection that elicited them; by constantly monitoring the density of the pathogenic community and spurring the expression of immune signalling molecules accordingly, AhR ensures that the host doesn’t spend the energy and resources bothering to clear the infection until it becomes threatening.
This was true in zebra-fish larvae, in mice, and in human cells in culture. Hopefully now that we know a bit more about how our cells spy on and exploit bacterial signals, therapies can be devised to target the most dangerous phases of an infection.