The common chronic obstructive pulmonary disease (COPD) is an increasingly important cause of morbidity and mortality. More than 200 million people worldwide are affected by COPD, making it the fourth leading cause of death. COPD is characterized by progressive destruction of the lung parenchyma, resulting in the development of emphysema, increased mucus production, and chronic airway inflammation. It is a highly heterogeneous disease. Cigarette smoke has been shown to be the most important risk factor for the development of COPD; but also burning of biomass fuels and occupational exposure are known to be COPD risk factors.
At Fraunhofer ITEM, we use primary cells, cell lines, fresh lung tissue, and animal models to induce features of COPD. Lipopolysaccharides (LPS), cigarette smoke, and cigarette smoke condensate are applied as agents. LPS-induced inflammation mimics primarily an acute and subacute inflammatory process in the lung. We have models of LPS-induced inflammation in laboratory animals including non-human primates, in fresh lung tissue and cells. Cells and tissue can also be exposed to cigarette smoke condensate and cigarette smoke. This is done primarily at the air-liquid interface. In particular the exposure of cells and tissue at the air-liquid interface is considered to closely reflect the human situation.