Researchers at the University of Liege in Belgium have discovered a new population of macrophages that are instrumental in repairing the pulmonary alveoli. This discovery could open the door to regenerative therapies for patients with respiratory viruses such as COVID-19.
Conditions like COVID-19 and other respiratory viruses can result in the destruction of large areas of the lungs, particularly the alveoli responsible for gas exchanges. Ineffective repair of these structures can lead to acute respiratory distress syndrome (ARDS) and cause a permanent reduction in the lungs’ ability to oxygenate blood.
A study from the GIGA Institute at the University of Liege published in Science Immunology found that atypical macrophages, which are characterized by specific markers and transiently recruited during the early recovery phase, play a beneficial role in regenerating pulmonary alveoli.
Coraline Radermecker, PhDUniversity of Liege, Belgium
“Our findings provide a novel and crucial mechanism for alveolar repair by these atypical macrophages,” said lead study author Coraline Radermecker, PhD, post-graduate researcher in the Department of Functional Sciences at the University of Liege. “We have detailed their characteristics, origin, location in the damaged lung, the signals they require to function and their role in tissue regeneration, specifically acting on type 2 alveolar epithelial cells, the progenitors of alveolar cells.”
The researchers wrote that the scientific community had previously overlooked these macrophages because they express a marker previously thought to be specific to another immune cell population — the neutrophils — and because they appear only briefly during the repair phase before disappearing.
“Our study highlights the reparative role of these macrophages, countering the prevailing idea that macrophages following respiratory viral infections are pathogenic,” added co-author Thomas Marichal, DVM, PhD, research professor at the University of Liege. “By targeting the amplification of these macrophages or stimulating their repair functions, we could develop therapies to improve alveolar regeneration and reduce complications from serious respiratory infections and ARDS.”
