What is it about?
A high surface tension can prevent normal lung inflation; to prevent this, the body synthesizes "lung surfactant", a detergent-like substance that lowers the surface tension in the alveoli. However, during inflammation that accompanies diseases such as Covid-19, the immune system secretes "lipases" that break down the lipids in bacterial and viral cell membranes, generating lysolipids that can compete with lung surfactant for the aveolar interface. These lysolipids can scrub lung surfactant from the interface by making the lung surfactant lipids soluble in body fluids which results in a higher surface tension and can prevent the lung from inflating uniformly. The effect of lysolipid is concentration dependent; below a threshold concentration, there is minimal effect, while above this threshold, the lung may go unstable.
Featured Image
Photo by National Cancer Institute on Unsplash
Why is it important?
Covid-19 infections result in damage to the lung surfactant producing cells, reducing the amount of available lung surfactant,. At the same time, the innate immune system produces lipases that break down bacterial and viral lipids to produce soluble lysolipid. If the lysolipid concentration reaches a certain level, the lungs can no longer inflate due to unbalanced surface tension forces. A significant fraction of deaths from Covid-19 were due to this acute respiratory distress syndrome that may result from this surface tension instability.
Perspectives
Read the Original
This page is a summary of: Evolution of interfacial mechanics of lung surfactant mimics progression of acute respiratory distress syndrome, Proceedings of the National Academy of Sciences, December 2023, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2309900120.
You can read the full text:
Resources
Contributors
The following have contributed to this page