(RxWiki News) Something harmless could turn deadly under the right circumstances. Researchers are beginning to understand how a harmless bacteria becomes a fatal infection in cystic fibrosis patients.
The bacteria, Burkholderia cenocepacia, has no effect on healthy humans but in cystic fibrosis patients, can cause severe lung infection that is resistant to most antibiotic treatments.
Researchers discovered that the bacteria affects how cells fight infections in cystic fibrosis patients. This new information can lead to new treatments targeting the bacteria.
"Ask your doctor about infections associated with cystic fibrosis."
The study was led by Amal Amer, MD, PHD, from Ohio State University. Researchers identified the bacteria affects the autophagy process of cells that are involved in fighting infections, called macrophages.
An existing drug, rapamycin, was effective in stimulating the autophagy process in macrophages in mice models with cystic fibrosis.
Autophagy is a normal process of cell development. Autophagy allows the starving cell to create energy by eating parts of itself. This can help cells focus on more important cell functions. Macrophages are a part of the immune system and are the first to appear during an infection.
Macrophages basically eat the bacteria that causes infection.
The infection caused by the Burkholderia cenocepacia bacteria is rare but highly contagious among cystic fibrosis patients and is fatal.
Focusing on macrophage cells, researchers discovered that inside the macrophage a molecule, called p62, plays a role in controlling the bacterial infection. Researchers believe that manipulating p62 levels in cystic fibrosis patients could help fight the infection.
In a related study, led by Basant Abdulrahman, a doctoral student at Ohio State University, rapamycin was tested on human and mice cells with the cystic fibrosis mutation.
Rapamycin is used to prevent donor organ rejection. The cells could not clear the bacterial infection on their own but rapamycin stimulated the autophagy process in macrophages which helped the cells fight the infection.
Researchers have identified two possible treatment targets for this deadly infection for cystic fibrosis patients. Future research would be needed to show how effective raising p62 levels is for fighting the infection.
Funding for the studies provided by the National Institutes of Health and the American Lung Association.
The study led by Dr. Amer was presented at the annual meeting of the American Society for Biochemistry and Molecular Biology. All results should be considered preliminary until published in a peer reviewed journal.
The study led by Mr. Abdulrahman was published in the November edition of Autophagy.
