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Study shows that airborne nanoparticles trigger autophagy in lung cells

New research from the Keck School of Medicine of USC shows that air pollution particles activate a cellular defense mechanism known as autophagy, which may reduce the ability of cells to fight off other harms. The findings were published in the journal Autophagy Reports.

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.

— Edward Crandall, PhD, MD, professor of pathology, member of the Hastings Center for Pulmonary Research and director of the Will Rogers Institute Pulmonary Research Center at the Keck School of Medicine of USC

In their research, Crandall and his team discovered a key step along the path between air pollution exposure and disease. Exposure to ambient nanoparticles limits the ability of cells to defend themselves against other potential harms.

Crandall, the study’s senior author, and his colleagues studied a cellular defense process known as autophagy, which cells use to destroy damaged or abnormal internal materials. 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 defense mechanism that has an upper limit, beyond which it can’t defend the cell any further.

—Edward Crandall

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. 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.

As part of the research, Crandall and his team also developed a new method of

studying autophagy, which can support future studies on the subject. They used a combination of fluorescent dyes and a powerful imaging method, known as confocal microscopy, to document the amount of autophagy taking place inside individual cells.

The new findings can help support ongoing research on autophagy, including for cancer treatment. 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.

Next, Crandall, Sipos and their colleagues will conduct further research to test whether adding nanoparticles to a cell directly increases its vulnerability to other threats, such as an infection. They plan to study the link in both healthy cells and cancer cells.

This work was supported by the Will Rogers Motion Picture Pioneers Foundation; Whittier Foundation; Hastings Foundation; and the National Institutes of Health [R01ES017034, U01HL108364, P01AG055367].


  • Arnold Sipos, Kwang-Jin Kim, Constantinos Sioutas & Edward D. Crandall (2023) “Kinetics of autophagic activity in nanoparticle-exposed lung adenocarcinoma (A549) cells,” Autophagy Reports, 2:1, doi: 10.1080/27694127.2023.2186568


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