Cystic fibrosis (CF) is a genetic disease that affects the lungs, pancreas, and other organs over time. A defective gene affects cells that produce mucus, sweat, and digestive juices. These fluids are normally thin and slippery; in people with CF, the cells secrete sticky, thick mucus.
When they are thick, these secretions clog airways and plugs tubes, ducts, and passageways. They trap bacteria, which causes recurring lung infections and increases the risk of chronic pneumonia. It also limits the ability to breathe over time. Mucus prevents the release of digestive enzymes in the pancreas, making it more difficult to break down food and absorb vital nutrients.
In a study published in the Journal of Bacteriology, researchers studied pseudomonas aeruginosa, the most common bacteria in CF patients, and identified the signal that controls when this bacteria starts producing biofilm. Biofilm is a group of microorganisms in which cells stick to each other and the surface they are on.
This film is extremely sticky and protects the bacteria from attack, which means that they are extremely difficult to get rid of. Neither immune responses nor antibiotics can reach bacteria once they are covered in biofilm, which allows the bacteria to grow and thrive.
Treatments targeting this signal would suppress the bacteria’s ability to make biofilm, destroying its first line of defense.
Prior to this study, researchers knew what signaling the bacterium uses to tell itself to form biofilm, but they didn’t know what molecular signals were telling the biofilm it was the time and place to cluster.
Now, they have identified the magnesium transporter MgtE as a key regulator of biofilm formation. MgtE is a protein on the surface of the bacteria that responds to abnormal levels of mucus—specifically, it responds to altered levels of magnesium. It responds to high levels of mucus by suppressing a signaling pathway that is involved in the formation of biofilm.
Researchers noted that chronic bacterial functions cause the gradual loss of lung function; cystic fibrosis itself does not cause the loss of lung function. These infections also cause difficulties with breathing, which results in serious strain on the lungs, cardiovascular system, and heart. Treatments aimed at reducing these infections would improve the quality of life and health outcomes for CF patients.
If you or a loved one lives with cystic fibrosis and could benefit from private duty nursing, call our Client Care Coordinators at (650) 462-1001 to learn more about NurseRegistry’s full range of services.
Kegel, Magdalena. “CF Lung Infection Discovery Could Lead to Way to Counter Bacteria.” Cystic Fibrosis News Today, 11 Oct. 2017, cysticfibrosisnewstoday.com/2017/10/11/lung-infection-discovery-could-lead-to-way-to-kill-the-bacteria-that-plague-cf-patients/
Chakravarty, Shubham, et al. “The Pseudomonas aeruginosa Magnesium Transporter MgtE Inhibits Type III Secretion System Gene Expression by Stimulating rsmYZ Transcription.” Journal of Bacteriology, 2017, jb.asm.org/content/early/2017/08/22/JB.00268-17.abstract
“Cystic Fibrosis Foundation.” About Cystic Fibrosis | CF Foundation, Cystic Fibrosis Foundation, www.cff.org/What-is-CF/About-Cystic-Fibrosis/
“What Is Cystic Fibrosis? What Causes It?” WebMD, WebMD, https://www.webmd.com/children/what-is-cystic-fibrosis – 1
“Cystic Fibrosis.” Mayo Clinic, Mayo Foundation for Medical Education and Research, 13 Oct. 2016, https://www.mayoclinic.org/diseases-conditions/cystic-fibrosis/symptoms-causes/syc-20353700