Interactions between bacteria that form deadly shields against the body’s natural defences could lead to new ways of treating antibiotic-resistant bacteria.
The bacteria Pseudomonas aeruginosa – which causes chronic lung infections – can communicate with each other to switch on production of molecules that kill white blood cells and prevent the bacteria from being eliminated by the body’s immune system.
Professor Michael Givskov from the Department of International Health, Immunology and Microbiology at the University of Copenhagen said: “Antibiotic resistance is one of the most serious emerging health problems in the world today. More than 70% of the disease-causing bacteria are resistant to at least one of the currently available antibiotics.” He collaborated on the study with the Technical University of Denmark, along with others in Denmark and the US.
P. aeruginosa is responsible for many hospital-acquired infections and causes chronic infections in those with pre-existing medical conditions such as cystic fibrosis. The bacteria cause persistent lung infections by forming a biofilm which spreads over the lungs. These biofilms are generally resistant to the host immune response and antibiotics.
The study – published in Microbiology – showed that P. aeruginosa uses quorum sensing to detect approaching white blood cells and warn other bacteria in the biofilm. These bacteria then increase their production of molecules called rhamnolipids which sit on the surface of the biofilm, forming a shield. White blood cells encountering the shield are then destroyed. Interrupting the quorum sensing to halt the shield response could be a way of treating the bacteria that can resist antibiotics and the host immune system.
“The ultimate goal [of this research] is to eradicate the present day’s antibiotic resistant bacteria that are involved in the bulk of chronic infections,” Professor Givskov said, “Studying interactions between P. aeruginosa and the innate and adaptive immune response will provide valuable information for the design of novel antimicrobials.”
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