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How the body repairs lung tissue after viral pneumonia

News 2024-25 EN

An international research team, led by lung researchers from Giessen, has discovered a new repair mechanism with therapeutic potential. The work has now been published in "Nature Communications."

How does the body repair damage to lung tissue after viral pneumonia, and how can these processes be therapeutically influenced? These are the questions addressed by an international research team led by Professor Dr. Susanne Herold, a lung and infection researcher at the Justus Liebig University Giessen (JLU), specializing in Internal Medicine, Infectiology, and Experimental Pneumology. Infections with respiratory viruses such as influenza viruses, which cause the flu, respiratory syncytial viruses (RSV), or coronaviruses can trigger viral pneumonia, which in severe cases can lead to lung failure. The researchers have identified a protein that mitigates lung damage caused by influenza viruses and could have therapeutic potential. The results have been published in the journal "Nature Communications."

Severe pneumonia is associated with a rapid decline in lung gas exchange, necessitating rapid regeneration of damaged lung tissue. Macrophages, also known as phagocytes, play an important role in the repair of inflammation-induced lung damage. They are a crucial component in the processes of immune defense, helping to eliminate pathogens from the body. There are two types: circulating macrophages, which can migrate to the site of infection through the bloodstream, and "resident" tissue macrophages, which are bound to specific tissues, such as alveolar macrophages in the lungs. Tissue-resident alveolar macrophages are long-lived cells in the lung's air sacs (alveoli), where gas exchange between blood and air occurs. They maintain stable conditions in lung tissue (tissue homeostasis) and are involved in the immediate defense against pathogens. Several studies have shown that during viral pneumonia, alveolar macrophages are depleted and gradually replaced by mobile macrophages originating from the bone marrow, which transform into alveolar macrophages in the inflamed lung.

The research team found that during the transformation process of mobile macrophages into alveolar macrophages, the protein Plet1 is produced to a high degree. Plet1 plays a crucial role in lung repair by inducing the proliferation of alveolar epithelial cells—specialized cells that line the lung's air sacs—and the resealing of this cell layer barrier. These positive effects could also be induced externally: administering Plet1 in a preclinical model mitigated viral lung damage and led to much faster recovery after severe infection, which would otherwise be fatal. "We have identified for the first time a factor that directly mediates the repair of damaged lungs. This finding underscores the therapeutic potential of Plet1 in combating severe lung damage caused by viral pneumonia, and possibly other forms of acute or chronic lung failure," said DZL scientist Prof. Herold.

The study involved scientists from various institutions specializing in infection and lung research, including the German Center for Lung Research (DZL), the German Center for Infection Research (DZIF), and the Instituto de Investigación en Biomedicina de Buenos Aires (IBioBA) in Buenos Aires, Argentina."


Original publication:

Pervizaj-Oruqaj, L., Selvakumar, B., Ferrero, M.R. et al. Alveolar macrophage-expressed Plet1 is a driver of lung epithelial repair after viral pneumonia. Nat Commun 15, 87 (2024).

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