Discovery Could Help Cystic Fibrosis Patients Get Rid of Bacteria That Attack Their Lungs
Researchers have identified a signal that controls when lung bacteria in cystic fibrosis patients start producing biofilm — a sticky secretion that protects them from attack and makes the bacteria virtually impossible to get rid of.
Since the signal suppresses bacteria’s biofilm-making machinery, the finding could lead to treatments that prevent bacteria from using this hard-to-break defense.
The study focused on the most common bacteria in cystic fibrosis patients — Pseudomonas aeruginosa.
“We know quite a lot about the regulatory signaling that is involved in the bacterium telling itself to form a biofilm, but we haven’t had much knowledge about the molecular signals that tell these organisms that it’s an appropriate time and place to cluster,” Gregory G. Anderson, a microbiologist at Indiana University-Purdue University Indianapolis, said in a press release.
“Specifically, we haven’t known what signals bacteria are receiving from the environment — in this case, the mucus in CF patients’ lungs — to tell them to form biofilms,” added Anderson, the lead author of the study.
Once bacteria start producing biofilm, neither immune responses nor antibiotics can reach them. This makes it the perfect environment to allow bacteria to grow.
In cystic fibrosis patients it is bacterial infections that cause the gradual loss of lung function, not CF itself, researchers noted.
Their study showed that a protein on the surface of the bacteria — the magnesium transporter MgtE — was a key regulator of biofilm formation.
The MgtE protein recognizes the bacteria’s chemical surroundings, including the abnormal levels of mucus found in the lungs of people with cystic fibrosis. The protein responds to altered levels of magnesium in particular. The research team’s experiments showed that MgtE suppressed the activity of a signaling pathway involved in the formation of biofilm.
“We have now tied MgtE, a protein in the membrane of bacteria, with known biofilm signaling networks,” Anderson said. “I think this is one of the first times such a link between an external signal and biofilm regulation has been identified.
“We are adding to the body of knowledge of biofilm formation with the ultimate goal of finding better ways to disrupt that formation, leading to improved treatments for the chronic pneumonia in CF patients,” he added.