Pseudomonas aeruginosa is a human pathogen which can cause life-threatening illness, especially in people who have a depleted immune system. One of the ways P. aeruginosa causes infection is through quorum sensing; a type of cell signalling pathway that initiates the production of virulence factors.
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P. aeruginosa is a gram-negative bacterium whose virulence depends on a large number of extra- and intracellular factors. Infections typically affect those in hospital (hospital-acquired infections), where there are strong selective pressures for more hardy, dangerous bacteria.
Quorum sensing
Quorum sensing involves the regulation of the expression of genes within the DNA of the bacterium, which is controlled by the cell-population density of the extracellular environment, or biofilm.
Cell signalling molecules called “autoinducers”, play a big role in altering gene expression. They act like switches, turning gene expression on and off depending on the number of bacteria in the population. Quorum sensing therefore allows for large, dense populations of bacteria to act in unison – almost like a ‘bacterial hive’.
P. aeruginosa Quorum sensing
Quorum sensing in P. aeruginosa has two different parts – the first being related to the expression of the gene encoding the protein LasB elastase. This is appropriately called the “Las system”, with this system containing the autoinducer ‘LasI’.
This system has also been known to activate genes related to secretory pathways. The second component of Quorum sensing in P. aeruginosa bacteria is called the “rhl system”, named due to its ability to control the gene expression which ultimately produces rhamnolipid. The autoinducer found inside this system is called rhlI, with this system also playing a role in producing LasB in an optimal manner.
In terms of human infection, the cell-to-cell interaction involved in Quorum sensing may have a role in enabling Pseudomonas aeruginosa to by-pass the host’s immune system. These bacteria already produce the endotoxins required to initiate disease, however, the coordinated expression of these virulence genes by whole, densely-packed populations allow for P. aeruginosa populations to effectively overcome the host defences, and cause infection at a more efficient rate.
Also, the production of biofilms – a complex collection of surface-associated bacterial cells, is a common cause of persistent infections, including P. aeruginosa infections. Biofilms have also been proven to be highly resistant to antimicrobials, as well as the actions of the host’s immune system.
P. aeruginosa Quorum sensing research
In a study performed in 2004, two different synthetic furanones were examined to find out their ability to cure lung infections in mice, by inhibiting Quorum sensing within the P. aeruginosa biofilms, which were causing the infection.
The study proved that furanones are able to successfully interact with the molecule N-acyl homoserine lactone, which in turn supresses P. aeruginosa biofilm Quorum sensing. This then accelerated the bacterial clearance inside the lungs of the mice, which significantly prolongs the lives of the mice that were tested.
This study was done to observe the ability to prevent cell-to-cell interactions, without killing the organisms. By using furanones to prevent quorum sensing and reduce biofilm formation, severe Pseudomonas aeruginosa infections could be more easily treated with antibiotics. This could help in preventing the average 400 deaths per year caused by P. aeruginosa in the United States.
Further Reading
Unraveling the survival strategies of Pseudomonas aeruginosa in lung infections