An international team of scientists has observed a previously unclear inflammatory mechanism caused by airborne particles that can worsen asthma symptoms. The paper is published in the journal Toxicological Sciences.
Research teams from Hiroshima University, the University of California and the Leibniz Research Institute identified a cell receptor—AhR—that was activated by these particles. This receptor promotes the production of inflammatory molecules to get rid of toxins in the body (such as fumes and diesel particles). It is found on cells in organs that are in contact with air, such as the skin, the gut and lungs. AhR’s function is to detoxify the body, but overactivation of this receptor can often cause health problems.
In their study, the group stimulated human and mice immune cells with diesel particles that activated AhR. The cells produced IL-33, a chemical messenger that promotes inflammation. To confirm that the levels of IL-33 were caused by AhR the researchers blocked signals from AhR in the cells and no IL-33 was found.
Small particles can bind to AhR and cause inflammation through immune cell activation. Credit: Yasuhiro Ishihara/Hiroshima University
The researchers concluded that AhR activation by airborne particles can make symptoms of diseases such as asthma more severe. Diesel fumes aggravate immune cells to release chemicals that promote inflammation.
Associate Professor Yasuhiro Ishihara of the Graduate School of Integrated Sciences for Life, Hiroshima University states that even though this is a promising finding and opens the door to a deeper understanding of the mechanisms of these diseases, the best way to avoid these is to “escape”. Even if you are not living right beside a factory or lots of vehicles, airborne particles can be distributed by the wind.
This is an urgent issue in our drastically developed world.—Prof. Ishihara
Yasuhiro Ishihara, Thomas Haarmann-Stemmann, Norman Y Kado, Christoph F A Vogel (2019) “Interleukin 33 expression induced by aryl hydrocarbon receptor in macrophages” Toxicological Sciences doi: 10.1093/toxsci/kfz114