Staph-Link Protein May Help Arthritis


Monday, June 24th 2002, 12:00 am
By: News On 6


WASHINGTON (AP) _ A protein that makes staph infections more dangerous by blocking the body's immune defenses may help point the way to better treatments for arthritis and other diseases.

The bacteria Staphylococcus aureus produces a protein that inhibits those defenses, thereby reducing the normal inflammatory response to infection, according to Dr. Triantafyllos Chavakis of Justus Liebig University in Giessen, Germany, and colleagues.

Reducing inflammation is crucial to combating arthritis and other diseases. The researchers suggest the action of the staph protein could form the basis for designing new anti-inflammatory drugs.

``Understanding the mechanisms by which bacteria avoid the host immune response might lead to novel therapies,'' Chavakis said.

The protein encourages staph to bind to host cells by connecting to receptors. Filling those receptors makes them unavailable to immune cells, whose movement to the site of the inflammation is then blocked.

The findings were being published Monday in the online edition of the journal Nature Medicine.

Dr. David A. Fox of the University of Michigan, who was not part of the research team, said that substances with anti-inflammatory properties often have applications beyond the body system in which they are initially studied.

Joint inflammation in rheumatoid arthritis depends on movement of white blood cells called leukocytes into the joint lining tissue, he noted, so blocking this migration could be a worthwhile strategy.

Staph is an extremely troublesome bacterium that leads to a variety of illnesses and is a major source of hospital-acquired infection. Staph causes such things as the scalded skin disease that strikes infants, toxic shock syndrome and systemic blood poisoning called sepsis.

Antibiotics once controlled the bacteria, but some strains of staph are now resistant to the drugs.

The German researchers found that while staph uses the protein known as extracellular adherence factor to block the immune defenses, the protein alone does not cause infection.

Reducing inflammation is a major focus of arthritis treatments. Also, in recent years, inflammation in the bloodstream has become a suspect in some heart disease.

Thus, the researchers suggest that it may be possible to use the protein in the development of molecules that could block immune system leukocytes from binding to cells, preventing the inflammation in affected areas.

The team tested that theory both in the lab and in mice infected with peritonitis _ inflammation of the abdominal cavity's lining _ and found that the protein reduced immune system response that would increase inflammation.

They now plan to develop and test synthetic molecules called ICAM-1 antagonists, designed to perform the same function. They potentially could be used in organ transplantation or rheumatoid arthritis, Chavakis said.

``It is very hard to define the time frame for such antagonists to be available in the clinic,'' he added.