A role for cardiolipin — an important component of mitrochondrial membranes in heart cells — in a mouse model of pneumonia is reported in a study published online this week in Nature Medicine. These findings could open the door for new therapeutic strategies aimed at modulating cardiolipin levels and its molecular interactions in human pneumonia.
Pneumonia is a leading cause of infectious deaths, though the mechanism by which bacterial pneumonia infects the lungs and leads to prolonged damage is unclear. Rama Mallampalli and colleagues found patients with pneumonia have elevated levels of cardiolipin, which may contribute to their lung damage.
The authors showed that a phospholipid transporter, ATP8b1, bound cardiolipin and internalized the lipid inside cells. However, mice with a mutant form of ATP8b1 that impairs cardiolipin uptake have elevated levels of the molecule in lung fluid — similar to patients with pneumonia. Since ATP8b1-mutant mice are prone to bacterial pneumonia, the authors state that this provides a new conceptual model for pneumonia and cardiolipin’s role in this disease.