If you’re a human being and old enough to be reading and understanding this blog—which I wholeheartedly hope is every single one of you, or else my logical reasoning skills are completely failing me—you’ve probably been host to Staphylococcus aureus. It’s one of the most common and successful bacteria on the planet, often causing boils or rashes on human skin, and sometimes picking up antibiotic resistance genes and killing patients in the form of MRSA.
In fact, statistically speaking, one out of every five of you have S. aureus on your person right this moment. Researchers have spent a lot of time trying to figure out what makes these bacteria so difficult for the human immune system to handle, and those efforts have shown some modest fruits in the past few years. But a new study from the University of Chicago identifies one strategy for bacterial survival that is especially cool.
Neutrophils are a type of white blood cell that ensnares invaders in neutrophil extracellular traps (NETs), a web-like structure of DNA and proteins. As one of the first lines of defense in the human immune response, they’re responsible for ensnaring troublesome bacteria that are then destroyed by amoeba-like white blood cells known as macrophages.
While neutrophils seem to have no problem netting themselves plenty of S. aureus when they begin their invasion, the battlefield is completely devoid of the all-important big-gun macrophages to finish them off. Somehow, the foreigners are defending themselves from the firing squad.
Researchers set to work to figure out how this happens by making a wide range of genetic modifications one-by-one to strains of S. aureus to discover which are important for their immune system avoidance. After narrowing it down to two genes that, when turned off, allow macrophages to thrive and do their job, the scientists set out to figure out what the hell the genes actually do.
As it turns out, the genes allow the bacteria to turn the netting against their own users. They discovered that S. aureus were converting NETs into 2’-deoxyadenosine (dAdo), a molecule that is toxic to macrophages. This effectively turned NETs into a weapon against the immune system.
“Sooner or later almost every human gets some form of S. aureus infection. Our work describes for the first time the mechanism that these bacteria use to exclude macrophages from infected sites,” said Olaf Schneewind, professor and chair of microbiology and senior author of the paper. “Coupled with previously known mechanisms that suppress the adaptive immune response, the success of these organisms is almost guaranteed.”
While the discovery is cool and all, don’t expect it to lead to the sudden development of new ways to fight the common bacteria. Both genes and the dAdo molecule are closely related to important human physiological mechanisms, and Schneewind believes targeting these in bacteria, without harming human function, could be difficult.
“In theory you could build inhibitors of these bacterial enzymes or remove them,” Schneewind said. “But these are untested waters and the pursuit of such a goal requires a lot more study.”
The study, “Staphylococcus aureus Degrades Neutrophil Extracellular Traps to Promote Immune Cell Death,” was published by Schneewind along with his University of Chicago colleagues Vilasack Thammavongsa and Dominique M. Missiakas.