Researchers Identify a Type of Immune Cells that Contribute to Lung Fibrosis

Researchers Identify a Type of Immune Cells that Contribute to Lung Fibrosis

Certain immune cells, called monocyte-derived alveolar macrophages, may contribute to lung inflammation and fibrosis, according to the results of a new study. Researchers believe that therapies targeting these monocyte-derived macrophages may improve fibrosis.

The study, “Monocyte-derived alveolar macrophages drive lung fibrosis and persist in the lung over the life span,” was published in The Journal of Experimental Medicine.

“This will be transformative for the field,” Alexander Misharin, MD, PhD, from Northwestern University and the study’s first author, said in a news release by Anna Williams. “Pulmonary fibrosis is a complex disease — it’s not driven by a single gene or cell type — but this study now demonstrates that these immune cells play a key role. This will change the current paradigm.”

It was generally believed that immune cells were not involved in the development of pulmonary fibrosis. However, previous studies at Northwestern suggested that immune cells may indeed play an important role in fibrotic processes.

To address this question, researchers followed the development of immune cells and their contribution to lung damage in animal models of pulmonary fibrosis by using modern genetic sequencing techniques.

They found that during fibrosis, monocyte-derived alveolar macrophages are recruited to the lungs and significantly express more profibrotic genes than normal alveolar macrophages residing in lung tissue. Furthermore, the genetic deletion of these cells prevented fibrosis in mouse models.

These results were confirmed in samples from patients with pulmonary fibrosis, in which increased levels of profibrotic proteins were found in monocyte-derived macrophages.

Based on these observations, the team suggested that targeting monocyte-derived alveolar macrophages may be a potential and valuable therapeutic avenue to tackle lung fibrosis in patients.

“This is a novel application of genomic technologies to understanding pulmonary fibrosis,” said Scott Budinger, one of the study’s principal investigators. “By showing that these technologies can be directly applied to patient samples, we offer the promise of incorporating them into personalized medicine approaches. It creates a resource for the research community to develop novel therapies.”

The next step is to further investigate the mechanisms underlying fibrosis in several inflammatory diseases, including pulmonary fibrosis, scleroderma, and rheumatoid arthritis, and advance the search for new antifibrotic therapies.

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