such as "Introduction", "Conclusion"..etc
May 27, 2009 — It appears that some superbugs have evolved to develop the ability to manipulate the immune system to everyone's advantage.
A team of researchers at The University of Western Ontario, led by
Joaquin (Quim) Madrenas of the Robarts Research Institute, has
discovered some processes that reduce the lethal effects of toxins from
superbugs, allowing humans and microbes to co-evolve. This discovery
may lead to novel alternatives to antibiotics that specifically target
the toxic effects of these superbugs.
Madrenas holds a Canada Research Chair in Immunobiology and is a
Professor of Microbiology & Immunology, and Medicine at the
Schulich School of Medicine & Dentistry at Western. He also is head
of Immunology at Robarts Research Institute and Director of the FOCIS
Centre for Clinical Immunology and Immunotherapeutics.
Staphylococcus (staph) aureus is the leading cause of infections in
hospitals and the second most common cause of infections in the general
population. By itself, it is linked to more than half a million
hospital admissions a year in North America with estimated costs of
more than $6 billion per year. Among the many weapons produced by this
superbug, the most potent and lethal ones are known as superantigens.
These lethal weapons cause massive and harmful activation of the immune
system that leads to Toxic Shock Syndrome (TSS). TSS is a very serious
disease that carries a high mortality, for which we do not have a
Scientists have been puzzled as to why, when the body is directly
exposed to the TSS toxins, a human can die within hours whereas
individuals may carry toxin-producing staph and not get sick or die.
What has the staph bug got that prevents the immune system of the
host from being kicked into high gear? Madrenas and his collaborators
at Western, Calgary and Chicago have identified the process that allows
the bug to stay in the body without causing that massive activation of
the immune system.
The secret lies in molecules found in the cell wall of staph. These
molecules bind to receptors known as TLR2 on immune cells of the host
triggering the production of a protein called IL-10, an
anti-inflammatory molecule that will prevent TSS.
"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" says Madrenas.
Based on these studies, Madrenas and colleagues have developed a
computer model that will help predict the outcomes of encounters
between staph and a host, and will reveal new aspects of these
The multidisciplinary team led by Madrenas includes David Heinrichs,
Ewa Cairns, Mansour Haeryfar, and John McCormick of the Departments of
Microbiology and Immunology, and Medicine at The University of Western
Ontario, as well as Paul Kubes from the University of Calgary and Gary
An from Northwestern University in Chicago.
The findings are being published in the journal Nature Medicine
and are available online May 24, 2009. The research was funded by the
Canadian Institutes of Health Research and the Kidney Foundation of
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