Health
Researchers identify genetic defects in alveolar macrophages that cause lung disease
New discoveries about the cause of PAP lung disease also offer solutions for treating obesity and heart disease. A research group led by Associate Professor Alexander Mildner at the University of Turku in Finland identified a genetic defect that causes lipid accumulation in the alveoli.
Alveoli are tiny bubble-like air sacs at the ends of the bronchi. It is essential for survival as it exchanges oxygen for carbon dioxide.
The alveoli are lined with a thin liquid membrane called surfactant, which is mainly composed of lipids. Surfactants not only protect the lungs from airborne pathogens and dust, but they also promote proper breathing by lowering the surface tension of the alveoli.
Surfactant lipids are constantly produced and removed from the alveoli. Alveolar macrophages, immune scavenger cells in the lung, degrade and recycle surfactant lipids. Defects in alveolar macrophage development and function lead to disturbed surfactant balance and pathological accumulation of surfactant lipids, ultimately leading to clogging of alveolar spaces. Accumulated lipids cause macrophages to swell and foam.
“This phenomenon can be observed in patients with alveolar proteinosis (PAP). They suffer from shortness of breath, impaired respiratory function and an increased risk of lung infections. This is a relatively rare disease. said Associate Professor Alexander Mildner of the University. He was leading research at the Max-Delbrück Center in Berlin, Germany, in collaboration with Professor Achim Leutz’s group, and his InFLAMES flagship program at the University of Turku, Finland.
Macrophages lack essential cellular tools
Disturbed gene regulation causes macrophage defects. Although one of these disorders has already been identified, Mildner and his group found that the lack of a second regulator prevented macrophages from clearing lipids in detergent.
This regulatory gene is the transcription factor C/EBPb. We observed that C/EBPb-deficient macrophages lack the cellular tools required for lipid clearance. ”
Alexander Mildner, Associate Professor, University of Turku, Finland
The significance of this discovery is not limited to PAP disease. Enlarged, foamy macrophages are also found in people with obesity and atherosclerosis.
“Maybe we can learn from alveolar macrophages in the lungs and translate our findings to other macrophages to help them digest lipids more effectively.” It may be possible to pharmacologically activate the EBPb-Pparg2 network, treat PAP or atherosclerosis, and promote lipid digestion in these cells. It may offer a new strategy for
sauce:
Journal reference:
Dörr, D., et al. (2022) C/EBPβ regulates lipid metabolism and Pparg isoform 2 expression in alveolar macrophages. scientific immunology. doi.org/10.1126/sciimmunol.abj0140.
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