Research published in Toxicological Sciences exposed a new mechanism whereby small toxic particles from diesel fumes can exaggerate the inflammatory response. The collaborative study was carried out by researchers in Japan, the US, and Germany, from Hiroshima University, the University of California and the Leibniz Research Institute.
Industrialization has increased the amount of man-made toxins in the air, and it has long been known that people who live in cities or industrialized areas are more prone to a wide range of respiratory diseases. Until this study, the underlying mechanisms were unclear.
The researchers identified a cell receptor called AhR that was activated by diesel particles. These receptors cover areas of the body that are in contact with the air, such as - the skin, gut, and lungs. The AhR receptor is designed to be activated when toxins reach the body, and as such, they trigger the process of detoxification of the body from airborne toxins (like fumes).
The researchers used both human and animal immune cells and subjected them to tiny particles of diesel fumes. In turn, the cells produced Interleukin 33 (IL-33), which is a protein that promotes inflammation as part of the immune response. They checked that the IL-33 was produced by AhR by blocking AhR, and found that no IL-33 was produced when AhR was blocked. Concluding that IL-33 is produced by AhR.
The researchers established how airborne particles from diesel fumes can exacerbate respiratory illness and make symptoms more severe, promoting inflammation. Lead researcher Ishihara stated, "This is an urgent issue in our drastically developed world." The key solution he said was to escape to the countryside to enjoy fresh air, with less airborne particles.
Related Biotics Research Products: