For years scientists have puzzled over why the intracellular pathogen Salmonella is able to survive—and thrive—in human and animal tissues, even within otherwise hostile cells that are part of the body’s immune system, such as white blood cells known as macrophages.
For years scientists have puzzled over why the intracellular pathogen Salmonella is able to survive—and thrive—in human and animal tissues, even within otherwise hostile cells that are part of the body’s immune system, such as white blood cells known as macrophages.
While multiple factors enable Salmonella to adapt to harsh conditions experienced during infection, a new Yale study reveals the molecular basis for the metabolic adaptations this pathogen undergoes that promotes its survival.
In an article published in the Proceedings of the National Academy of Sciences, a team of Yale researchers identify the process—including the role of a key signaling molecule that helps regulate carbon uptake in these organisms—that underlies the physiological changes governing Salmonella’s carbon source preference during infection.
Their findings also show that the behavioral changes commonly observed in Salmonella in laboratory settings don’t necessarily reflect how they behave in the natural environment, said Eduardo A. Groisman, the Waldemar Von Zedtwitz Professor of Microbial Pathogenesis at the Yale School of Medicine and senior author of the study.
They also offer new insights into the role of metabolism in antibiotic tolerance, the researchers say.
