CHAMPAIGN, Ill. By better understanding how antimicrobials bind and thereby get inactivated in the mucus of air passages, researchers at the University of Illinois may have found a way to help cystic fibrosis patients fight off deadly infections.
While not a cure, this work has potential as a therapeutic strategy against bacterial infections in cystic fibrosis, said Gerard Wong a professor of materials science and engineering, of physics, and of bioengineering at the U. of I., and a corresponding author of a paper accepted for publication in the Proceedings of the National Academy of Sciences. The paper is to be posted this week on the journals Web site.
Ordinarily, pulmonary passages are lined with a thin layer of mucus that traps bacteria and other pathogens. Moved along by the motions of countless cilia, the mucus also acts as a conveyor belt that disposes of the debris. In patients with cystic fibrosis, however, the mucus is more like molasses thick and viscous. Because the cilia can no longer move the mucus, the layer becomes stuck, and the bacteria grow, multiply and colonize. Long-term bacterial infections are the primary cause of death in cystic fibrosis.
Using synchrotron X-ray scattering and molecular dynamics simulations, the researchers took a closer look at the mucous mess.
Debris in the infected mucus includes negatively charged, long-chained molecules such as mucin, DNA and actin (from dead white blood cells). It turns out most of the bodys antimicrobials, such as lysozyme, are positively charged.
We found that actin and lysozyme two of the most common components in infected mucus form ordered bundles of aligned molecules, which is something you dont expect in something as messy as mucus, said Wong, who also is a researcher at the universitys Beckman Institute. Held together tightly by the attraction of opposite charge, these bundles basically lock up the antimicrobials so that they are unable to kill bacteria.
|Contact: James E. Kloeppel|
University of Illinois at Urbana-Champaign