The rise of antibiotic-resistant bacteria has initiated a quest for alternatives to conventional antibiotics. One potential alternative is PlyC, a potent enzyme that kills the bacteria that causes strep throat and streptococcal toxic shock syndrome. PlyC operates by locking onto the surface of a bacteria cell and chewing a hole in the cell wall large enough for the bacteria's inner membrane to protrude from the cell, ultimately causing the cell to burst and die.
Tesearch has shown that alternative antimicrobials such as PlyC can effectively kill bacteria. However, fundamental questions remain about how bacteria respond to the holes that these therapeutics make in their cell wall and what size holes bacteria can withstand before breaking apart. Answering those questions could improve the effectiveness of current antibacterial drugs and initiate the development of new ones.
Researchers at the Georgia Institute of Technology (Gabriel Mitchell, Prof. Kurt Wiesenfeld, and Prof. Joshua Weitz) and the University of Maryland (Prof. Daniel Nelson) recently conducted a study to try to answer those questions. The researchers created a biophysical model of the response of a Gram-positive bacterium to the formation of a hole in its cell wall. Then they used experimental measurements to validate the theory, which predicted that a hole in the bacteria cell wall larger than 15 to 24 nanometers in diameter would cause the cell to lyse, or burst. These small holes are approximately one-hundredth the diameter of a typical bacterial cell.
More information in the article available online at the Journal of the Royal Society Interface