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MHH research team investigates how messenger substances from fatty tissue impair gas exchange in the alveoli
Most people know that smoking is bad for the lungs. What is probably less well known is that a lack of exercise and an unhealthy diet can also damage the lungs and promote long-term conditions such as chronic obstructive pulmonary disease (COPD) or asthma. The “Lifestyle factors in respiratory health and disease” project is now investigating the influence of diet, tobacco smoke and exercise on lung health in different phases of life and how they change the interaction between the lungs and other organs at a molecular level. All five sites of the German Centre for Lung Research (DZL) are involved. A team led by PD Dr Julia Schipke, a scientist at the Institute of Functional and Applied Anatomy at Hannover Medical School (MHH) and the DZL site BREATH Hannover, is investigating the role of nutrition and physical activity. In particular, the researchers want to decipher the communication between adipose tissue and the lungs in early childhood and adult obesity. The DZL is funding the project with a total of 760,000 euros.
Gas exchange made more difficult
The focus is on adipokines. This is a group of messenger substances produced by fatty tissue that signal to the brain when we are full, for example. They are also associated with the development and progression of obesity-related comorbidities such as type 2 diabetes. However, adipokines could also influence lung tissue, particularly the alveoli, as they are known technically. The alveoli are lined with alveolar epithelial cells, of which the type 2 epithelial cells (AT2) form what is known as surfactant. This substance reduces the surface tension - just like the detergents in washing-up liquid reduce the surface tension of water. This allows the alveoli to unfold easily and remain open, so that gas exchange between the blood and alveoli is possible and the lungs are evenly ventilated. “Too much carbohydrate and fat in the diet changes the surfactant production and the lipid balance in the AT2 cells and ensures that the vessels in the blood-air barrier thicken and the alveolar walls are less elastic, which makes gas exchange more difficult,” explains PD Dr Schipke.
Testing results in human cell cultures
It is known from clinical studies that birth weight and diet predict the risk of impaired lung function in later life. In the project, PD Dr Schipke and her team now want to use a mouse model to clarify the effects of an unhealthy diet high in sugar and fat in the early and late stages of life. “Some animals will have access to a running wheel so that we can also test whether and how physical activity is suitable for counteracting the harmful effects on the lungs,” says the biologist. After all, our muscle cells also produce messenger substances known as myokines. And these seem to have the potential to improve lung health. However, it is still unclear exactly how this happens.
“We now want to find out which molecular and structural changes take place in the lungs and which messenger substances control these processes in detail,” says PD Dr Schipke. The researchers then want to test the adipokines and myokines identified in the mouse model in cell cultures of human lung cells and lung slices from explanted organs. “Mice and humans are very comparable in this case because they have a similar surfactant system and their metabolism also reacts similarly to an unhealthy diet,” says the scientist. The researchers want to find new biomarkers that influence the airways and especially the pulmonary alveoli. In the long term, the results could improve the early detection of lung damage caused by obesity and enable new treatment strategies to combat changes in the lungs.
SERVICE:
For further information, please contact PD Dr Julia Schipke, schipke.julia@mh-hannover.de.
A symbolic photo.
Copyright: Karin Kaiser/MHH/Photoshop-KI generated.
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