Heart disease is the leading cause of death in many countries, and smoking is one of its biggest risk factors.
Doctors have advised people to quit smoking for decades, but scientists have continued searching for the exact biological changes that connect cigarettes with damaged arteries. New research provides one of the clearest explanations yet.
A research team from the University of Oklahoma discovered that cigarette smoke can turn helpful immune cells into drivers of chronic inflammation. The study, published in Circulation Research, found that this process speeds up the buildup of plaque inside arteries, increasing the risk of heart attacks and strokes.
The investigators used a mouse model of atherosclerosis, a disease in which fatty deposits narrow and harden the arteries. They closely examined how immune cells responded after exposure to cigarette smoke.
They found that neutrophils, which normally rush to fight infections, became unusually active after contact with cigarette smoke. Instead of simply protecting the body, these cells entered blood vessels in large numbers and interacted with macrophages, another important immune cell.
When the neutrophils died, they released powerful inflammatory signals. These signals disrupted the normal work of macrophages, preventing them from removing dead cells and excess cholesterol. Without this cleanup process, harmful material accumulated more easily inside artery walls.
Over time, these fatty deposits can become unstable. If a plaque breaks open, it may trigger the formation of a blood clot that blocks blood flow to the heart or brain. This is one of the main causes of heart attacks and ischemic strokes.
The study also produced an unexpected finding. Tobacco chemicals caused similar immune changes even when they were given by mouth instead of being breathed into the lungs. This indicates that once these chemicals enter the body, they may directly affect immune cells wherever they circulate.
The researchers say these findings could eventually open the door to new treatments aimed at reducing inflammation in smokers and former smokers. Current therapies mainly focus on lowering cholesterol, but inflammation is increasingly recognized as another major cause of cardiovascular disease.
Future research will investigate which specific chemicals in cigarette smoke are responsible for the harmful immune response. The team also plans to examine whether vaping devices and nicotine pouches trigger the same changes and to confirm the findings in human studies.
This research strengthens the evidence that smoking damages far more than the lungs by disrupting the body’s own immune defenses.
Although quitting smoking remains the most effective protection, the study offers valuable insight that may help scientists develop better treatments for cardiovascular disease in the future. Because the work was performed in animals, clinical studies in people will be essential before new therapies are developed.
If you care about heart health, please read studies about how eating eggs can help reduce heart disease risk, and herbal supplements could harm your heart rhythm.
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Source: University of Oklahoma.
