Researchers have for the first time described a method that Staphylococcus aureus (staph) infection uses to inactivate the body’s immune system. A protein produced by the staph bacteria causes previously healthy B cells — a specialized cell of the immune system — to commit suicide, a process called apoptosis. “By the targeted elimination of disease-causing B cells, properly dosed injections of SpA may have the potential to control the over-activity of the immune system that causes damage in autoimmune diseases like lupus and in certain cancers,” said Gregg Silverman, M.D., UCSD professor of medicine and senior author of the paper. From the Alliance for Lupus Research:STAPH INFECTION PROCESS LEADING TO B CELL SUICIDE
DESCRIBED FOR FIRST TIME
Enhances Potential for Future Development of B-Cell Based Therapy for Lupus
New York, May 5, 2003 — Researchers at the University of California, San Diego — supported by the Alliance for Lupus Research and the National Institutes of Health — have for the first time described a method that Staphylococcus aureus (staph) infection uses to inactivate the body’s immune system. A protein produced by the staph bacteria causes previously healthy B cells — a specialized cell of the immune system — to commit suicide, a process called apoptosis. The research will be published in the May 5 issue of the Journal of Experimental Medicine and at http://www.jem.org/pap.shtml on April 28.
In the new study, the researchers found that SpA, a staph protein, functions as a B cell toxin in mice. The protein attaches to a receptor on B cells, eventually causing the B cells to turn on themselves in a suicide process.
Researchers believe that B cells play a major role in tissue damage that occurs in lupus. “By the targeted elimination of disease-causing B cells, properly dosed injections of SpA may have the potential to control the over-activity of the immune system that causes damage in autoimmune diseases like lupus and in certain cancers,” said Gregg Silverman, M.D., UCSD professor of medicine and senior author of the paper.
“The significance of Dr. Silverman’s research is that the discovery that injections of SpA limit the activity of B cells in animals allows us to proceed to the next step, to test the protein’s usefulness in people,” said John H. Klippel, MD, scientific director of the Alliance for Lupus Research, which funded this study. “If results hold true for people, SpA may eventually prove to be an effective treatment for lupus.”
In addition to Silverman, the study was conducted by the paper’s co-author Carl S. Goodyear, Ph.D., a UCSD postdoctoral researcher.
The study was funded by the National Institutes of Health and the Alliance for Lupus Research. The ALR was founded by Robert Wood Johnson IV, of the Johnson & Johnson healthcare family and owner of the NFL’s New York Jets, with the Arthritis Foundation to raise the profile and scope of lupus research. Since its inception in 1999, the Alliance has committed more than $24 million to research, and has made remarkable gains toward unlocking the mysteries of this disease. ALR directs 100 percent of funds raised to peer-reviewed research and scientific programs. It recently received the highest rating (four stars) from Charity Navigator, an independent resource that evaluates the effectiveness and financial health of more than 2,300 charities.
For more information on lupus and the Alliance for Lupus Research,
a 501 (c) (3) organization, visit http://www.lupusresearch.org or call (800) 867-1743.
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Gave this more thought. What I’m wondering is this: at least 3 different viruses (HHV-6, MSRV, Epstein-Barre) have been implicated and four major MS types have been identified. Yet no firm proof has yet been found that directly convicts anyone of these viruses. This suggests that there may be other factors involved in the infection process. Let’s assume like this latest lupus theory suggests that a bacterial infection kicks off first, affecting the immune system response…then a virus attacks, causing the actual damage to nervous system. It might explain the difficulty in pinning a culprit down in the case of MS.
In the case of lupus, there may only be the single punch, caused by staph or someother opportunistic infection in concert with highly local environmental conditions. This may explain identified lupus clusters. It would be interesting to see if there’s any change in incidence in MS in those same cluster areas.
It sounds as if staph has a similar modus operandi as HHV-6 or MSRV in multiple sclerosis.
Perhaps there’s a link — staph infection suppresses immune system while HHV-6 opportunistically imbeds itself in nervous system? Food for thought.