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Funk Lab

Ageing & Environmental stress in lung disease

The Funk laboratory aims to understand how ageing and environmental stress affect the homeostasis and regenerative capacity of the lung epithelium, thereby promoting chronic inflammatory diseases, such as COPD. Based on this, we want to identify molecular mechanisms and targets in epithelial cells as a basis for therapeutic approaches. Our preferred research tools are innovative 3D lung organoid models from primary mouse and patient-derived tissue.

The Funk laboratory aims to understand how ageing and environmental stress affect the homeostasis and regenerative capacity of the lung epithelium, thereby promoting chronic inflammatory diseases, such as COPD. Based on this, we want to identify molecular mechanisms and targets in epithelial cells as a basis for therapeutic approaches. Our preferred research tools are innovative 3D lung organoid models from primary mouse and patient-derived tissue.

Vision

Ageing and environmental insults are important risk factors for chronic inflammatory diseases, including COPD (Chronic obstructive pulmonary disease) in the lung. However, how they influence and potentially facilitate each other towards disease development is not yet well understood. To this end, we investigate the following overlaps between the hallmarks of ageing and environmental insults to identify mechanistic links and processes:

  • Stem cell capacity & regeneration
  • Epigenetic alterations
  • Altered intercellular communication & dysbiosis

Deciphering these relationships could offer a unique opportunity to develop preventive and age-specific therapeutic approaches for COPD patients. Furthermore, in view of the progressive ageing of our society and the increasing pollution of our environment, the medical need for effective treatment of chronic inflammatory diseases is one of the central issues of future healthcare; we want to contribute to this with our research.

Research

Our research focusses on the epithelial cells of the lung. We aim to uncover at the molecular level how ageing and environmental stress affect the homeostasis of the lung epithelium, its regenerative capacity and its intercellular interaction properties. In particular, we aim to decipher molecular pathways and mechanisms associated with the following questions:

  • How does ageing sensitize the lung epithelium to environmentally-induced damage?
  • Which environmental stressors have the potential to induce age-related phenotypes?
  • How do age- and environmental stress-induced changes in epithelial cells affect their interaction with immune cells?
  • How is the gut-lung axis affected during ageing and upon environmental stress?

In the next step, we want to modify the identified mechanisms in epithelial cells and create the basis for therapeutic approaches.

Tools & Techniques

To achieve our research goals, we use innovative 3D lung organoid models generated from primary mouse or patient-derived tissue. To reconstruct the epithelial interaction interface with the environment and the cellular microenvironment ex vivo, we are advancing our organoid models by micro-injection and as co-culture systems. To gain mechanistic insights, we perform high-throughput transcriptomic and epigenomic analyses, drug screenings, and CRISPR/Cas9-based genome engineering approaches.

Picture right: Lung airway organoid. Multiciliated cells are marked by acetylated alpha-tubulin (green).
Source: Maja Funk/DKFZ Heidelberg 

Contact

Porträt Maja Funk

Dr. Maja Funk

Junior Group Leader