A new study sheds light on how cells infected with Pseudomonas aeruginosa can sense the pathogen and decide whether to fight back or not. The research also provides vital information for the development of alternatives to antibiotics.
Pseudomonas aeruginosa is a gram-negative bacterium that inhabits soil and water. It is an opportunistic pathogen, which means it causes disease primarily in people who have a compromised immune system.
Those at risk include people living with cystic fibrosis and those staying in healthcare settings.
What makes this bacterium particularly challenging is that it is resistant to a range of antibiotics.
How do our cells defend themselves against P. aeruginosa infection? And what can scientists do to tackle multi drug resistant strains?
Bacteria can use a sophisticated method called
The system provides them with information on the density of the bacterial colony and which other bacterial species are present in their surroundings.
Quorum sensing relies on signaling molecules called autoinducers. Bacteria release these into their environment to send messages to each other.
A host of bacterial processes depend on quorum sensing. These include the formation of biofilms and the secretion of virulence factors, both of which can cause a significant threat to our health.
Writing in the journal Science, Pedro Moura-Alves and Stefan Kaufmann from the Max Planck Institute for Infection Biology in Berlin in Germany explain how infected cells can intercept P. aeruginosa autoinducers, allowing them to choose the best method of defense.
Medical News Today spoke to Professor Kaufmann about the research.
He explained that “P. aeruginosa is an important nosocomial pathogen with high antimicrobial resistance. Nosocomial pathogens are often resistant to antimicrobials (antibiotics). Nosocomial infections are typically acquired in hospitals.”
“At the same time, P. aeruginsoa is a ubiquitous microbe in the environment, and it can be found in washbasins, etc. It is likely people get into contact with P. aeruginosa frequently, however, at low doses when they are not harmful,” he continued.
“In contrast, if they grow up to higher abundance, they switch on their gene program, which enables them to attack the host because now they produce virulence factors.”
In a previous study published in
For their current research, the team used a combination of human cells, zebrafish, and mice, to show that AhR can detect quorum sensing autoinducers.
“We were surprised to find that the Aryl Hydrocarbon Receptor is able to spy on bacterial communication language, translating it into host defence terms,” Moura-Alves, who now works at the Ludwig Institute for Cancer Research at the Oxford University in the United Kingdom, told MNT.
“This allows the host to monitor infection and to react accordingly to the level of threat.”
The team write in the paper:
“We propose that by spying on interbacterial communication, AhR is capable of sensing the status quo of the P. aeruginosa community during infection, allowing the host to mobilize the most appropriate defense mechanism according to the severity of threat.”
Disrupting quorum sensing is one way that scientists are trying to address the threat of multi drug resistant P. aeruginosa infections.
“By interfering with bacterial growth and modulating host response more precisely, our findings can help us and others to develop better (more precise) novel intervention measures,” Professor Kaufmann explained to MNT.
While such alternatives may be a long way off in the future, the team’s new insights into how the bacteria communicate with each other should help with this strategy.