Who is the first dead cell discovered?
Dead cells cause inflammation
HEIDELBERG. The chronic inflammation of the airways in cystic fibrosis is not only caused by bacteria.
Dead cells that have fallen victim to the lack of oxygen in the airways clogged with mucus are also likely to trigger a violent reaction of the immune system.
Scientists from the Center for Translational Lung Research Heidelberg have shown this for the first time in mice with a lung disease comparable to cystic fibrosis, reports the Heidelberg University Hospital.
They also found out which signaling pathway triggers this immune reaction and how it can be blocked: a drug that is approved for the treatment of rheumatic joint inflammation also suppresses inflammation caused by the dead cells in the mouse model (Am J Respir Crit Care Med. 2015; online January 21).
Inflammation without bacterial contamination
So far, doctors have assumed that chronic inflammation of the airways in cystic fibrosis and other chronic obstructive pulmonary diseases such as COPD is predominantly the result of an infection with bacteria or viruses.
Recent studies from Australia made suspicious: Infants with cystic fibrosis had an inflammation of the airways in the first few months of life, but often no bacterial infestation was detectable.
"We know inflammations from other organs that are not caused by an infection with pathogens. They occur, for example, after a heart attack or stroke, when cells in the heart or brain perish due to a lack of oxygen," explains Professor Marcus Mall, Medical Director of the Translational Department Pneumology at the Center for Translational Lung Research Heidelberg (TLRC), in the notification of the Heidelberg University Hospital.
The messenger substance interleukin-1 (IL-1), which is released from the dying cells and triggers an immune response, plays an important role in this "germ-free" inflammation.
The scientists have now for the first time also detected this messenger substance in the lung tissue of mice with a chronic lung disease comparable to cystic fibrosis.
"The mucus plugs in the airways lead to a lack of oxygen in the lung sections behind them. Cells then die there," says Mall.
"The worse the mucus, the more dead cells." In the diseased lungs, cells continuously suffocate, so the inflammation never stops.
In mice with cystic fibrosis-like lung disease, which, due to a genetic change, lacked the receptor for IL-1, there was hardly any inflammation in the lungs despite the mucus.
With them, the signal path failed, the dying cells did not trigger an immune response. The lung function was retained and life expectancy improved significantly, the message says.
For Mall this means: "This newly discovered disease mechanism around interleukin-1 may play a decisive role in the chronification and progression of lung disease in cystic fibrosis and COPD. This opens up new treatment options."
There is already a suitable drug against the new inflammatory mechanism: The active ingredient anakinra is injected in chronic inflammatory diseases such as rheumatoid arthritis and blocks the IL-1 receptor.
In adult mice with chronic lung disease, the drug alleviates inflammation and thus reduces the destruction of lung tissue.
Whether anakinra is also effective as an anti-inflammatory therapy in patients with cystic fibrosis has yet to be investigated in clinical studies. (eb)
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