The role of these enzymes, called COX enzymes, is not yet understood completely, and
medications that inhibit them may have adverse side effects. Recent research has discovered that drugs that inhibit COX enzymes, such as COX-2, have an impact on the effectiveness of vaccines. This new research indicates that inhibiting COX-1, which is present in tissues
throughout the body, such as the brain or kidneys, could also impact vaccines' effectiveness.
"If you're taking aspirin regularly, which many people do for cardiovascular treatment, or acetaminophen (Tylenol) for pain and fever and get a flu shot, there is a good chance that you won't have a good antibody response," said Charles Brown, associate professor of veterinary pathobiology in the MU College of Veterinary Medicine.
"These drugs block the enzyme COX-1, which works in tissues throughout the body. We have found that if you block COX-1, you might be decreasing the amount of antibodies your body is producing, and you need high amounts of antibodies to be protected."
The researchers also are studying the regulation of inflammation and how that leads to the development or prevention of disease. Many diseases, such as arthritis, cardiovascular disease and diabetes, are all chronic inflammatory diseases. Contrary to previous beliefs, inflammation is generally a good thing that helps protect individuals from infection. Many of the non-steroidal drugs that treat inflammatory conditions reduce antibody responses, which are necessary for treating infections.
"So far, we've tested this on an animal model and have found that these non-steroidal drugs do inhibit vaccines, but the next step is to test it on humans," Brown said. "If our results show that COX-1 inhibitors affect vaccines, the takeaway might be to not take drugs, such as aspirin, Tylenol and ibuprofen, for a couple weeks before and after you get a vaccine."
Citation: Blaho, Victoria A., Buczynski, Matthew W., Dennis, Edward A., Brown, Charles R. Cyclooxygenase-1 Orchestrates Germinal Center Formation and Antibody Class-Switch via Regulation of IL-17. The Journal of Immunology, 2009, doi: 10.4049/jimmunol.0901499