As a postdoctoral fellow, Dr. Richardson continued studying bacterial metabolism in the context of its interaction with host innate immunity. He showed that host-production of nitric oxide (NO), a broad-spectrum immune effector, targeted multiple metabolic enzymes inhibiting the growth of pathogenic bacteria. In contrast, he found that the human pathogen Staphylococcus aureus, unlike all other tested bacteria including coagulase negative staphylococci, was able to resist the cytotoxic effects of host NO and thrive in its presence. S. aureus NO-resistance was shown to be essential for full virulence and hinged on the ability of the bacterium to evoke a metabolic state inherently resistant to the effects of this immune radical.
In 2008, Dr. Richardson established his laboratory at the University of North Carolina at Chapel Hill, focusing on the metabolic adaptations of S. aureus to host immunitywork that was soon featured as a Science cover article. Richardson's research studies how the availability of host arginine affects the outcomes of S. aureus infections. While the host converts free arginine to NO in response to inflammatory stimuli, arginine can also be converted to a class of compounds known as polyamines under similar conditions. S. aureus can resist the effects of NO, but for unknown reasons certain species of polyamines are lethal to the pathogen. Dr. Richardson's laboratory studies the battle between the host and S. aureus over the fate of free arginine. Mark Smeltzer, University of Arkansas for Medical Sciences, calls his work "both insightful and scientifically compelling, without exception."
Richardson's late graduate mentor, Igor Stojilijkovic, summarized Richardson to Fang: "He has a big brain, but his heart is even bigger. He is one of those rare individuals who you know will make it in any endeavor he chooses to follow."
|Contact: Garth Hogan|
American Society for Microbiology