Questions raised about painkillers
ommonly used medications like ibuprofen and Celebrex may reduce the body's ability to make antibodies, which are crucial for proper function of the immune system, according to a report by University scientists published in the Journal of Immunology.
Although it is well known that non-steroidal anti-inflammatory drugs like ibuprofen and the newer Cox-2 selective drugs such as Celebrex or Bextra effectively fight inflammation by altering the function of many different types of cells, this is the first time scientists have shown a direct connection between the popular painkillers and B lymphocytes, or white cells known as B cells.
The report, whose lead author is graduate student Elizabeth Ryan, shows that human B cells highly express the Cox-2 enzyme, and that blocking the enzyme activity reduces the B cells' ability to make antibodies.
The Cox-2 connection to B cells has both positive and negative implications for the immune system, according to corresponding author Richard Phipps, professor of environmental medicine and of microbiology and immunology. The primary role of B cells is to make the antibodies that lock onto infectious bugs and fight them off. The cells also serve as the immune system's memory by recognizing and eliminating germs that have attacked previously.
For example, when a person is vaccinated the goal is to promote an immune response by making antibodies to protect against a certain illness. But if the vaccinated patient takes a Cox-2 selective inhibitor, or an non-steroidal anti-inflammatory drug such as Advil or aspirin, to ease pain at the injection site, the drug could reduce the amount of antibody produced by the vaccine. In the military, where soldiers receive multiple vaccines, the problem could be greater, Phipps says.
"Drugs that target the Cox enzymes play an important role in blunting inflammation and fever," Phipps explains. "However, inflammation and fever are normal aspects of the human immune system. Blocking these pathways during initial vaccination or infection may reduce our ability to produce antibodies that protect us."
On the other hand, the use of drugs that inhibit the Cox-2 enzyme might be a potential therapy for diseases involving too many abnormal B cells, such as non-Hodgkin's lymphoma, where the goal is to stop their proliferation, or in autoimmune diseases that are marked by abnormal antibody production, adds Phipps.
At this point, the research group has demonstrated the B-cell connection to Cox-2 in studies of healthy human cell samples, in vitro, and in defective mice that lack the Cox-2 enzyme. Researchers say the next step is to begin clinical trials to study the antibody production in healthy people who receive vaccines.
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