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Ozone produced by antibodies during bacterial killing and in inflammation

Professor Richard A. Lerner, M.D., Associate Professor Paul Wentworth, Jr., Ph.D., and a team of investigators at The Scripps Research Institute (TSRI) is reporting that antibodies can destroy bacteria, playing a hitherto unknown role in immune protection. Furthermore, the team found that when antibodies do this, they appear to produce the reactive gas ozone.

"[Ozone] has never been considered a part of biology before," says Lerner, who is Lita Annenberg Hazen Professor of Immunochemistry and holds the Cecil H. and Ida M. Green Chair in Chemistry at TSRI. The report will appear in an upcoming issue of the journal Science.

The ozone may be part of a previously unrecognized killing mechanism that would enhance the defensive role of antibodies by allowing them to subject pathogens to hydrogen peroxide and participate directly in their killing. Previously, antibodies were believed only to signal an immune response.

This ability of antibodies to generate toxic compounds may also link them to a number of inflammatory diseases, such as atherosclerosis, lupus, multiple sclerosis, and rheumatoid arthritis. Furthermore, this research opens up exciting possibilities for new antibody-mediated therapies for conditions ranging from bacterial and viral infection to cancer.

Recognition and Killing in the Same Molecule

Also called immunoglobulins, antibodies are secreted proteins produced by immune cells that are designed to recognize a wide range of foreign pathogens. After a bacterium, virus, or other pathogen enters the bloodstream, antibodies target antigens--proteins, fat molecules, and other pieces of the pathogen--specific to that foreign invader. These antibodies then alert the immune system to the presence of the invaders and attract lethal "effector" immune cells to the site of infection.

For the last hundred years, immunologists have firmly held that the role of antibodies was solely to recognize pathogens and signal
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Contact: Jason Bardi
jasonb@scripps.edu
858-784-9254
Scripps Research Institute
14-Nov-2002


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