COPD: Cigarettes block self-healing

Christiane Fux studied journalism and psychology in Hamburg. The experienced medical editor has been writing magazine articles, news and factual texts on all conceivable health topics since 2001. In addition to her work for, Christiane Fux is also active in prose. Her first crime novel was published in 2012, and she also writes, designs and publishes her own crime plays.

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The lungs can repair damage on their own - normally. This no longer works for people with chronic obstructive pulmonary disease (COPD). The smoke from cigarettes in particular blocks the self-healing mechanisms. But this destructive process can possibly be stopped.

So far there is no cure for the lung disease COPD - on the contrary. Once the disease is there, it progresses inexorably. Researchers at the Helmholtz Zentrum München have now discovered a central mechanism that is responsible for the destruction of lung tissue. And they have found a way to switch it off - at least in laboratory experiments with cell cultures.

Blocked self-healing

The lungs of non-smokers are also constantly damaged - by pathogens or fine dust, for example.That is why natural self-healing takes place continuously in the healthy respiratory organ. The basis for this is the so-called Wnt / beta-catenin signaling pathway in the lung cells. "Why it is blocked in the case of COPD was previously unclear," explains Dr. Melanie Königshoff from the Helmholtz Center Munich.

Smoke changes the cell surface

Together with her team, she came across the molecule Frizzled-4 during their investigations. “Frizzled-4 is what is known as a receptor. It sits on the surface of lung cells, where it controls their self-renewal via Wnt / beta-catenin, ”explains first author Wioletta Skronska-Wasek. "If the cells are exposed to cigarette smoke, Frizzled-4 disappears from the surface and cell regeneration comes to a standstill."

The researchers were able to demonstrate this using cell cultures, among other things. The authors also found that without the receptor, certain proteins that are important for the elasticity of the lungs, including elastin, fibulin and IGF1, were lost.

Restored recovery

To check their results, the scientists artificially stimulated the production of Frizzled-4 in a cell culture experiment. This enabled the blocked signal path and thus the self-healing ability of the cells to be reactivated. The elasticity proteins were also increasingly produced again.

This is a good starting point for further research and future therapies for COPD, say the researchers. The study was preceded by observations by the team that Frizzled-4 was significantly less common in the lung tissue of COPD patients and in particular of smokers than in non-smokers.

Almost always fatal

Cough, sputum and shortness of breath - these are the typical signs of COPD. There are no exact figures, but estimates assume that ten to twelve percent of adults over 40 years of age in Germany suffer from the lung disease, which in many cases is fatal. Even if there are some non-smokers among COPD patients, it is mainly smokers who are affected.

Source:

Skronska-Wasek, W. et al .: Reduced Frizzled receptor 4 expression prevents WNT / ß-catenin-driven alveolar lung repair in COPD. American Journal of Respiratory and Critical Care Medicine, doi: 10.1164 / rccm.201605-0904OC

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