Evolution of interfacial mechanics of lung surfactant mimics progression of acute respiratory distress syndrome.

Autor: Ciutara CO; Department of Chemical Engineering and Materials Science, University of Minnesota, Minneapolis, MN 55455., Iasella SV; Department of Chemical Engineering and Materials Science, University of Minnesota, Minneapolis, MN 55455., Huang B; Department of Chemical Engineering and Materials Science, University of Minnesota, Minneapolis, MN 55455., Barman S; Department of Chemical Engineering and Materials Science, University of Minnesota, Minneapolis, MN 55455., Zasadzinski JA; Department of Chemical Engineering and Materials Science, University of Minnesota, Minneapolis, MN 55455.
Jazyk: angličtina
Zdroj: Proceedings of the National Academy of Sciences of the United States of America [Proc Natl Acad Sci U S A] 2023 Dec 19; Vol. 120 (51), pp. e2309900120. Date of Electronic Publication: 2023 Dec 12.
DOI: 10.1073/pnas.2309900120
Abstrakt: How acute respiratory distress syndrome progresses from underlying disease or trauma is poorly understood, and there are no generally accepted treatments resulting in a 40% mortality rate. However, during the inflammation that accompanies this disease, the phospholipase A 2 concentration increases in the alveolar fluids leading to the hydrolysis of bacterial, viral, and lung surfactant phospholipids into soluble lysolipids. We show that if the lysolipid concentration in the subphase reaches or exceeds its critical micelle concentration, the surface tension, γ, of dipalmitoyl phosphatidylcholine (DPPC) or Curosurf monolayers increases and the dilatational modulus, [Formula: see text], decreases to that of a pure lysolipid interface. This is consistent with DPPC being solubilized in lysolipid micelles and being replaced by lysolipid at the interface. These changes lead to [Formula: see text] which is the criterion for the Laplace instability that can lead to mechanical instabilities during lung inflation, potentially causing alveolar collapse. These findings provide a mechanism behind the alveolar collapse and uneven lung inflation during ARDS.
Competing Interests: Competing interests statement:The authors declare no competing interest.
Databáze: MEDLINE
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