Sunday, 30 March 2014

Prickly protein helps stop Staphylococcus

A genetic mechanism that controls the production of a large spike-like protein on the surface of Staphylococcus aureus bacteria alters the ability of the bacteria to form clumps and to cause disease, according to a new study.

Under normal conditions, Staphylococcus bacteria interact with proteins in human blood to form aggregates, or clumps. This clumping behavior has been associated with pathogenesis -- the ability of bacteria to cause disease. However, the mechanisms that control clumping are not well understood.

In the process of investigating how staph bacteria regulate cell-to-cell interactions, researchers at the UI Carver College of Medicine discovered a mutant strain of staph that does not clump at all in the presence of blood proteins.

Further investigation revealed that the clumping defect is due to disruption of a genetic signaling mechanism used by bacteria to sense and respond to their environment. The study shows that when the mechanism is disrupted, the giant surface protein is overproduced -- giving the cells a spiny, or "porcupine-like" appearance -- and the bacteria lose their ability to form clumps. Furthermore, the research team found that this clumping defect also makes the bacteria less dangerous in an experimental model of the serious staph infection, endocarditis.

For further details, see:

Jennifer N. Walker, Heidi A. Crosby, Adam R. Spaulding, Wilmara Salgado-Pabón, Cheryl L. Malone, Carolyn B. Rosenthal, Patrick M. Schlievert, Jeffrey M. Boyd, Alexander R. Horswill. The Staphylococcus aureus ArlRS Two-Component System Is a Novel Regulator of Agglutination and Pathogenesis. PLoS Pathogens, 2013; 9 (12): e1003819 DOI: 10.1371/journal.ppat.1003819

Posted by Tim Sandle