Researchers have discovered that blocking a protein called interleukin-11 (IL-11) can reverse scarring in Idiopathic Pulmonary Fibrosis (IPF).
IPF is a type of lung disease which causes scarring of the lungs, known as fibrosis. Over time, the fibrosis gets increasingly worse so that it becomes hard for those with the condition to get the oxygen they need, making it difficult to carry out day to day activities.
Currently there are two drugs, pirfenidone and nintedanib, which can help slow the rate at which the disease progresses. There is currently no treatment that can stop or reverse scarring that has already formed in the lung.
However, recent research on mice may be paving the way towards a new approach for the treatment of IPF.
Where it began
In 2013, Professor Toby Maher and Dr Elizabeth Renzoni, respiratory consultants at the Trust, made the novel discovery that patients with IPF had increased levels of the IL-11 protein in lung cells known as fibroblasts, responsible for producing scar tissue.
At the time it was unclear what role the increased IL-11 had in IPF but in 2017 it was discovered that increased levels of IL-11 causes lung fibroblasts to become highly active and to destroy the lung, causing it to scar and not function properly.
Professor Stuart Cook, head of the Cardiovascular Genetics and Genomics at the National Heart & Lung Institute, Imperial, led a team of researchers to answer; if IL-11 could be blocked, would it help prevent the process of lung fibrosis?
Using mice models the researchers administered drugs, known as therapeutic antibodies, which attach to IL-11, effectively blocking its activity. The researchers found that not only did the drugs reduce damage to the lungs but it also reversed scarring that had already formed.
So, what does this mean for patients?
The research has only been conducted in mice so far, but according to Professor Maher, one of the author on this research, there’s hope for patients;
“Idiopathic respiratory failure is a terrible disease with an untreated life expectancy of 3 years. Although we have treatments to slow disease progression, we desperately need new therapies to genuinely transform outcomes for people with IPF. This exciting research highlights the importance of IL-11 in driving the development of fibrosis and gives hope for a new treatment approach to halt and maybe even reverse the devastating lung scarring of IPF.”
Professor Maher said, explaining the importance of this research for patients.
The research was conducted in collaboration between Imperial College London, Medical Research Council London Institute of Medical Sciences, Duke-NUS Medical School and National Heart Centre Singapore.
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