New York: The link between air pollution and lung disease has long been recognised. A new study reveals a biological process that may be behind that link - a discovery which could provide new insights on better ways to treat or prevent diseases related to pollution exposure. The study found that exposure to ambient nanoparticles, or very small pollutants in the air, activates a cellular defence mechanism known as autophagy, which may reduce the ability of cells to fight off other potential harms.
This may help explain why air pollution increases a person's risk for a number of acute and chronic lung diseases, including lung cancer, interstitial pulmonary fibrosis, and chronic obstructive pulmonary disease. "We know that diseases, especially lung diseases, can result from air pollution exposure. What we don't know are the mechanisms by which that occurs," said Edward Crandall, Professor of pathology, at the Keck School of Medicine of University of Southern California (USC).
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For the first time, the researchers found that, when exposed to nanoparticles, autophagy activity in cells seems to reach an upper threshold. "The implication of these studies is that autophagy is a defence mechanism that has an upper limit, beyond which it can't defend the cell any further," Crandall said.
In the study, published in the journal Autophagy Reports, the researchers conducted a series of tests using lung adenocarcinoma cells. They first exposed the cells to nanoparticles, then to rapamycin (a chemical known to stimulate autophagy), then to both nanoparticles and rapamycin.
In every case, autophagy activity reached the same upper threshold and did not increase further. Consequently, cells may lack the ability to further boost autophagy to defend against other dangers, such as smoke inhalation or a viral or bacterial infection. While autophagy is a boon for healthy cells, it makes cancer cells harder to destroy. Developing methods to raise or lower autophagy in cells could be a key way to protect against and treat disease, the team said. (IANS)
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