Their findings explain a critical survival tactic of a pathogen that causes more skin and heart infections than any other microbe, and kills more than 100,000 Americans every year.
Senior author Victor J. Torres, PhD, assistant professor of microbiology, said that what they've found is that Staph unleashes a multi-purpose toxin capable of killing different types of immune cells by selectively binding to surface receptors.
Torres said that staph has evolved the clever ability to target the immune system at different stages.
Their most recent work solves this puzzle, showing for the first time how receptors on neutrophils (a common type of white blood cell) also enable binding of the LukED toxin.
The researchers found that LukED latches onto surface receptors called CXCR1 and CXCR2, creating the same deadly pores that it does when it latches onto CCR5 receptors. "The mechanism is the same," says Dr. Torres. "The strategy makes Staph deadlier in mice."
Neutrophils are the first responders. Upon infection, they race through the bloodstream to kill off the invading pathogen.
Torres said that they are like the marines of the immune system.
T-cells, macrophages and dendritic cells rush in later, mounting a secondary attack to help the body clear the pathogen and remember it in the future.
Torres added that killing off the first responders completely disarms the immune system.
The study has been published in the journal Cell Host and Microbe.
--ANI (Posted on 20-10-2013)