Good and bad lipids in the lung

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Entry by Angelo Mao, AP 225, Fall 2010

Title: Good and bad lipids in the lung

Authors: Kong Chen and Jay K Kolls

Journal: Nature

Volume: Vol 16(10)

Pages: 1078-1079


The normal healthy lung requires the presence of surfactants on the inside of each alveolus (also called the lumen space) to reduce the surface tension. Without a reduction of surface tension within the alveolus, the balance of pressure from inside and outside the alveolus would be such that the alveolus would collapse, leading to an inability of the lung to facilitate gas exchange as well as physiological problems like fibrin deposition. Alveolar collapse can result from numerous traumas, but in this study, researchers tie the maintenance of surfactant levels in the alveolus to a phospholipid cardiolipid, to the action of a transport protein ATP8b1.

Soft Matter keywords: surfactant, surface tension, lipid


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This Nature article is an overview of several experiments, and one in particular, that were performed to elucidate the respective roles of ATP8b1 and cardiolipid. Researchers had shown that cardiolipid, a host-derived molecule, actually disrupts surfactant activity. They also found that increased levels of cardiolipid were correlated with occurrences of pneumonia in mice and human subjects. Previous research had shown that ATPb81 is a member of a protein transport lipid family that, when mutations occur, lead to increased risk for pneumonia. A recent study demonstrated that ATPb81 played a role in removing cardiolipid from alveolar space: overexpression of ATPb81 decreased cardiolipid levels in the lung and increased survival to experimental pneumonia, whereas gene knockout of ATPb81 in an in vitro cell line led to decreased cardiolipid intake. This strongly suggests that ATPb81 is an active protein transport involved in removing cardiolipid from the alveolar space. What is unknown, however, is why cardiolipid is produced by the host body if it leads to increased risk to pneumonia and alveolar dysfunction. How it disrupts the function of the surfactants, which are mixtures of phospholipids and proteins and contained within its own lipid bilayer, is also unknown, although it would not be surprising if this disruption were caused by cardiolipid binding to the surfactant on the hydrophilic end, changing the energetics of their grouping, or on the hydrophobic end, destroying their surfactant capabilities altogether.


1. Ray, N.B. et al. Nat. Med. 16, 1120–1127 (2010).