Jan. 20 (UPI) -- Researchers at the University of Illinois at Urbana-Champaign and Newcastle University in England have uncovered how a unique bacterial enzyme prevents the immune system from fighting infections.
The team of investigators used the antibiotic-resistent form of the bacterium Staphylococcus aureus, the "superbug" methicillin-resistant S. aureus, or MRSA, to determine how the bacteria can resist immune system attacks to survive treatment.
S. aureus has mutated to survive nutritional immunity, which prevents bacteria from getting key nutrients it needs to survive.
Nutritional immunity deprives S. aureus of manganese, the metal used by the bacterial enzyme superoxide dismutase, or SOD.
SOD works as a shield to reduce the damage from oxidative burst. Combined with nutritional immunity, the two weapons normally work to weaken and kill bacteria. S. aureus differs from other types of bacteria, however, in that it contains two SOD enzymes. The second SOD enzyme strengthens the bacteria's ability to resist nutritional immunity.
"Our immune system is very effective and prevents the majority of microbes we encounter from causing infections," Thomas Kehl-Fie, professor of microbiology at the University of Illinois and co-author of the study, said in a press release. "But pathogens such as S. aureus have developed ways to subvert the immune response. This realization is both exciting and perplexing, as both SODs were thought to utilize manganese and therefore should be inactivated by manganese starvation."
Researchers found that the second staphylococcal SOD was able to use manganese and iron, when it was previously thought it could only use manganese.
The study showed that when S. aureus was starved of manganese by the body, the bacteria activated cambialistic SOD using iron instead.
"The cambialistic SOD plays a key role in the bacterium's ability to evade the immune defense," Kevin Waldron of Newcastle University and co-author of the study, said in a press release. "Importantly, we suspect similar enzymes may be present in other pathogenic bacteria. Therefore, it could be possible to target this system with drugs for future antibacterial therapies."
The study was published in PLOS Pathogens.