Mitochondrial structure, integrity and function in inflammatory diseases

Debilitating fatigue is common in patients with autoimmune, inflammatory and infectious diseases.

Immune responses require massive amounts of energy and mitochondria are responsible for generation of ATP from oxidation of nutrients.

This organelle also activates immune cells via the release of nucleic acids, phospholipids, metabolites and reactive oxygen species.

Release of such signals is essential for killing pathogens but when produced in excess can also drive chronic inflammatory responses.

The central role of mitochondria in regulating immune responses forms the basis for a new hypothesis where mitochondrial sensitivity towards stressors associated with modern life (e.g. obesity, pollutants) is a missing link explaining the increased prevalence of immunological diseases. However, this hypothesis lacks mechanistic evidence.

This project aims to improve current understanding of the structure, biophysical properties and functional regulation of mitochondria in human immune cells, as well as the delicate balance between energy production, life-saving protection from pathogens and devastating inflammatory disease.

A new research field will be created where multidiciplinary studies of mitochondrial structure (Testa), biophysical properties (Sezgin) and function (Rorbach) are integrated into studies of human cells, from individuals with/without immune disease (Brodin), which together hold promise for development of new and combined technologies, not usually considered together.