Some of the world's most lethal superbugs, such as the methicillin-resistant Staphylococcus aureus (MRSA) bacteria, have the ability to start generating large amounts of toxins inside the host organisms, namely in humans, once they infect them. When that happens, the immune systems of sufferers become highly active, and the patients risk dying from what is known as the Toxic Shock Syndrome (TSS). However, it would appear that some MRSA strains have learned to coexist with their human hosts, preventing the release of the toxins even though they still produce it.
At this point, with MRSA being the largest source of infection in US hospitals, and the second most serious country-wide, finding a new treatment against it is one of researchers' greatest priorities. An estimated $6 billion goes to caring for MRSA patients every year, and a cure or preventive strategy against the bacteria could save the federal government some serious money, to be invested in other health care reforms and health care programs.
In a new investigation, researchers from the University of Western Ontario, led by Joaquin Madrenas, have managed to pinpoint the exact mechanisms that MRSA uses to keep its host alive. The spectacular find could help scientists create novel types of therapy for the condition that do not specifically target the bacteria, but its effects on the immune system instead. Madrenas is the Chair in Immunobiology at the UWN Robarts Research Institute, and also a Professor of Microbiology, Immunology, and Medicine at the Schulich School of Medicine & Dentistry,
PhysOrg reports.
“It is clear that staph superbugs have developed strategies to control the toxicity of its lethal superantigen toxins, thereby preventing TSS. We believe that this is an important mechanism that warrants continued investigation. It also illustrates that evolution may operate not only by competition but also by networking ultimately leading to peaceful co-existence,” the expert said.
According to the results of the new study, published online in the latest issue of the scientific journal Nature Medicine, a number of molecules in MRSA's cell walls bind to certain receptors on immune system cells, known as TLR2. When this happens, the cells produce the anti-inflammatory protein IL-10, which plays a crucial role in preventing TSS. By working on better understanding and mimicking this organism, experts could potentially save thousands of lives in the long run.