Why do Bacterial Ills Often Follow Flu? Scientists Find Possible Answer.
Albany, N.Y., April 28, 2008 - An Albany Medical College research team has discovered a possible reason why bacterial infections are more likely to develop in the week or so following an infection from the flu. Further, in animal experiments, they have shown a way to stop it from happening. Their work is reported in the journal Nature Medicine (advance online publication – April 27).
Pediatricians, pulmonologists and critical care doctors are all too familiar with patients who develop secondary bacterial infections (i.e. bronchial and lung infections, ear infections, pink eye) about a week after they come down with a virus, including the flu. These bacterial infections can, in fact, be much more serious than viruses. For instance, during flu pandemics, including the infamous 1918 outbreak, at least half of the people who die succumb to secondary bacterial infections, not the flu itself. However, despite years of research, this phenomenon has not been understood. Now, lab experiments at Albany Medical College using mice have shown that a molecule called interferon, that is involved in the immune mechanism the body uses to clear the virus, inadvertently shuts down the body’s normal defenses against bacteria.
“Cells called alveolar macrophages are present in the lungs and normally are at the ready to help clear bacteria out. However, we found that when the immune system is activated by a virus, the interferon that is part of that process actually ‘turns off’ alveolar macrophages and thus increases susceptibility to bacteria which then have a chance of getting in and proliferating,” explained Dennis Metzger, Ph.D., professor, Theobald Smith Alumni Chair, and director of the Center for Immunology and Microbial Disease at Albany Med. Dr. Metzger and Research Associate Keer Sun, Ph.D., are the authors of the paper in Nature Medicine. Dr. Metzger says the alveolar macrophage function is turned off just about a week after infection with a virus, the same time bacterial infections tend to take hold.
Dr. Metzger says as the body diverts all its attention toward fighting the virus, interferon actually changes the properties of the bacterial fighting cells, leaving them defenseless. “It changes those cells for its own purposes in fighting a viral infection and then inadvertently shuts down the body’s bacterial fighting system,” he said, pointing out this is a temporary phenomenon. Things return to normal after a week or so, but not before bacterial infections have been given a “window of opportunity,” Dr. Metzger explained.
In further experiments, the scientists figured out a way to prevent interferon from shutting down the bacteria-fighting immune system. They looked toward antibodies, which are proteins produced by the immune system that can render certain substances useless. For instance, chickenpox antibodies render the chickenpox virus useless. Likewise, an interferon antibody would block interferon’s activity. So, they found that by treating virus-infected mice with an interferon antibody and rendering interferon useless, bacteria fighting cells were not affected and the mice did not develop secondary bacterial infections.
“Yet even without the help of interferon, the immune system was still able to properly fight off the virus, leading us to think that maybe interferon is not playing a central role in anti-viral immunity,” explained Dr. Metzger.
Albany Medical College holds a provisional patent on this method of treatment, which Dr. Metzger says has the potential in the future of becoming a medical treatment to prevent secondary bacterial infections.
“Especially with growing antibiotic resistance, a treatment that can be given that would actually prevent a bacterial infection, thus negating the need for antibiotics, would be quite welcome in our society,” he said. “If it works in humans, this treatment would involve giving an antibody (which is different from an antibiotic) in a pill or injection or spray at the first sign of a viral infection like the flu.”
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Beth Engeler