Cholesterol Drugs could Increase Infection Risk
New research suggests that cholesterol lowering drugs might destroy the body's ability to fight infection. Statin drugs work well to lower cholesterol, but in a study, researchers found that simvistatin impairs the function of infection fighting cells called macrophages.
Simvistatin was also found to increase the production of cytokines that are inflammatory chemicals released in the body in response to infection. The result of increased cytokine production found from the cholesterol lowering drug could lead to sustained and worsening inflammation.
Cosima T. Baldari, Ph.D., a scientist from the Department of Evolutionary Biology at the University of Siena in Siena, Italy who assisted with the study says, "Our understanding of how these drugs affect the immune system should help maximize the benefits of these excellent drugs." Cholesterol lowering drugs are a mainstay for preventing and treating heart disease, but in the current study conducted on human and mouse cells, simvistatin was found to lower the body's ability to fight infection.
The scientists first grew human cells then exposed them to Staphylococcus areus, found on the skin and in the lungs. They used healthy macrophages from humans and mice that normally "gobble' bacteria. Once the bacteria grew, they observed the response of the immune cells treated with simvistatin.
The macrophages treated with simvistatin were not able to kill and digest bacteria compared to untreated cells.
The simvistatin treated cells also produced more cytokines that can make inflammation worse. John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology says, "Statins are lifesavers, but there might be room for improvement. Studies like this help pave the way for researchers to develop newer versions of drugs like statins that are more specific for their intended effect increasing the benefits of these pharmaceuticals."
Cholesterol lowering drugs are beneficial, but might hinder the ability of the body to fight infection, found in the new study.
Journal of Leukocyte Biology. 2010;87:433-442