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A new UCLA Health study in mice has identified a new potential trigger for pulmonary fibrosis: lipid dysregulation (a fat imbalance) within alveolar macrophages. These are the immune cells that serve as the first line of defense against pathogens and tissue damage. Under normal conditions, they are essential for the maintenance and repair of the lung's airspaces. However, when these cells suffer from a lipid imbalance, they lose their protective qualities, malfunction and begin actively promoting disease.

The paper is published in the American Journal of Respiratory Cell and Molecular Biology.

Lipid-filled macrophages, cells filled with too much fat, have previously been observed in lungs with pulmonary fibrosis, but this has generally been considered a result of the disease rather than a potential cause of it.

Pulmonary fibrosis is a debilitating lung disease with limited options for therapy. It is characterized by progressive scarring of lung tissue, ultimately leading to respiratory failure and high mortality rates. The question of what triggers pulmonary fibrosis has remained largely unsolved.

Previous UCLA studies researching the cholesterol metabolism of macrophages found that lipids detectable in the lungs of patients with other severe pulmonary diseases (autoimmune pulmonary alveolar proteinosis and idiopathic pulmonary fibrosis) were directly associated with disease burden and decreased lung function.

This led researchers to investigate whether lipid accumulation typically associated with pulmonary fibrosis isn't merely a consequence but one of the triggers of the disease.

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