Researchers from the University of Oklahoma have discovered a previously unknown immune mechanism that shows how smoking accelerates the formation of fatty plaques in the arteries and increases the risk of blood clots and strokes.
Experiments conducted by scientists on laboratory mice showed that cigarette smoke activates neutrophils (immune cells that are the first responders to infection), causing a sharp increase in their numbers within the bloodstream. Once activated, these cells interact with other immune cells known as macrophages, leading to the death of the neutrophils and the release of proteins that inhibit macrophage function. As a result, the body's ability to clear blood vessels of dead cells and harmful cholesterol is reduced, paving the way for the formation of blood clots and strokes.
To the researchers' surprise, they found that this immune inflammation occurs even when the chemicals in the smoke enter the body through pathways other than the lungs, indicating the ability of toxic compounds to directly affect immune cells after being absorbed into the bloodstream.
The researchers believe that these findings open new horizons for understanding why smoking is one of the most dangerous factors causing cardiovascular disease, and pave the way in the future for developing innovative treatments that not only lower cholesterol, but also curb chronic inflammation within blood vessels.
Many studies indicate that smoking is a major cause of many diseases, such as cardiovascular diseases and digestive system diseases. One study also showed that smoking increases the likelihood of developing type 2 diabetes.
