Inflammatory Reaction to Fine Dust Particles
Fine dust particles have long been suspected of causing or aggravating cardiovascular and respiratory diseases in humans. But what specific reactions in the respiratory tract do these particles trigger? Two scientists in Munich, Assistant Professor Matthias Wjst and Professor Holger Schutz, searched for an answer to this question. In their study, they exposed mice for several hours to ultrafine carbon particles. The amount of particulate was about ten to a hundred times the concentration that is measured in large cities with a lot of pollution. Microscopic and molecular analyses showed that the reaction in the lung caused by fine dust particles occurs in two phases. This process is typical for inflammation.

Heightened gene activity
Fine dust consists of particles with a diameter of maximally 100 nanometers. In comparison: a human hair is between 100,000 and 200,000 nanometers thick. In the experiment of Wjst and his team, the mice inhaled such fine carbon particles. Then the scientists flushed cells out of the respiratory tract. In mice that had inhaled the ultrafine particles for four hours, they discovered that the number of specific inflamed cells (polymorphous granulocytes) were slightly elevated. At the same time the scientists detected a heightened activity of the genes containing the blueprint for so-called heat shock proteins. These are proteins which keep other proteins functioning in extreme situations. They are considered to be signs of a first stress reaction of cells.

If the mice breathed the dust particles for 24 hours, genes were active that are associated with inflammatory reactions. The immune cells and tissue cells of the investigated lungs produced neurotransmitters that attract the body’s own macrophages and which activate additional immune cells. These neurotransmitters include osteopontin, lipocalin-2 and galectin-3. Furthermore, the production of collagen, a structural protein of the lung connective tissue, was stimulated. What is interesting about these findings is that these reactions also appear in severe lung diseases such as fibrosis of the lungs, sarcoidosis and lung cancer and are a typical sign for inflammatory changes. Even if the researchers found no morphological change of the lung tissue, they assessed the heightened gene activity for heat shock proteins and additional immunomodulatory proteins as expression of a mild inflammatory reaction due to inhaled fine dust particles.

The research team of Wjst and Schulz, which is funded by the Federal Ministry of Education and Research (BMBF) within the framework of the National Genome Research Network (NGFN), is confident that osteopontin, lipocalin-2 and galectin-3 can serve as useful markers for further studies on the effects of particulate burdens. Two of the three noticeably elevated proteins, osteopontin and lipocalin-2, also play a role in the development of arteriosclerosis. “It is not yet clear whether our results with mice are transferable to humans. If so, this could perhaps explain why fine dust particulate has an adverse effect on the health condition of people with cardiovascular diseases,” surmised Dr. Elisabeth André, one of the scientists involved in the research.
 
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