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Bye, Bye Biofilms

As free-swimming Pseudomonas aeruginosa bacteria colonize the lungs of cystic fibrosis (CF) patients, they cluster together into biofilm communities. Biofilms are far more resistant to antibiotics than bacteria in the free-swimming, planktonic form. Now DMS researchers, led by physiologist Bruce Stanton, Ph.D., have determined that a mutation in the CF gene causes airway cells to release more iron, which in turn stimulates the formation of biofilms. After reporting their findings recently in the American Journal of Physiology: Lung Cellular and Molecular Physiology, they have begun exploring whether iron chelators (which remove excess iron), used in conjunction with antibiotics, would have a synergistic effect in killing the bacteria.

In this video, filmed through a confocal microscope, a combination of the iron chelator conalbumin and the antibiotic tobramycin is used on P. aeruginosa that have been grown on CF airway cells. The live bacteria are stained with a green fluorescent protein. But they turn red as the combination therapy kills them. To learn more about the recent CF and biofilms studies, read "Hunting down gray tornadoes in the lungs." And for a feature-length article on Bruce Stanton's CF research, read "Battling the CF Monster."

Bruce Stanton and his collaborators study antibiotic-resistant biofilms in the lungs of cystic fibrosis patients.


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