20 November 2014
Pulmonary fibrosis is caused by scarring that thrives on itself, with the tougher, less elastic tissue replacing the lung, making it more and more difficult for patients to breathe. It's unknown whether the tissue in the organ is directly damaged or whether immune cells trigger the scarring process.
Finding the answer to this is important for developing future treatment for the incurable condition, but new research has shown that both these processes could play a key role.
Indicating a new direction for therapies of the future, the study looked at a model of lung fibrosis and found that fat cells - or lipids - gathered in the areas of the lung where oxygen is absorbed. Although lipids often serve as useful lubrication and help keep the lungs inflated, the team found excessive levels within the organ.
The research, which is published in the American Journal of Respiratory Cell and Molecular Biology, found that cells produce lipids as a response to stress and dumped them into the lungs.
This excess fat then reacts with oxygen to form fat that acts as an inflammatory signal, and is then devoured by immune cells called macrophages. The new study found that, when full of oxygen-rich fat cells, the macrophages activate a healing process to heal the wounded tissue, but this also leads to the development of fibrotic lung disease.
Posted by Edward Bartel
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