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Prof. Dr. Marcus Mall

BIH- und Einstein-Professor, Klinikdirektor

Kontaktinformationen
Anschrift:Charité - Universitätsmedizin Berlin
Augustenburger Platz 1

13353 Berlin

Kontakt für Anfragen

Marina Birr
Assistentin der Klinikleitung

Augustenburger Platz 1
13353 Berlin, Germany
+49 (0)30 450 566 182
marina.birr@charite.de

CF is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene and remains the most common fatal genetic disease in Caucasian populations. In healthy airways, CFTR encodes a cAMP-regulated anion channel that plays a key role in epithelial anion (Cl- and HCO3-) and fluid secretion. In the CF lung, CFTR dysfunction causes dehydration and acidification of airway surfaces, which leads to abnormal viscoelastic properties of the mucus and impairs important airway defence functions such as mucociliary clearance (MCC) and bacterial killing. These defects trigger a pathogenetic cascade of mucus plugging, chronic neutrophilic inflammation, infection and progressive structural lung damage that that remains the main cause of death in patients with CF.

Over the past 20 years, the Mall lab has made several contributions to our current understanding of the pathogenesis of CF lung disease and the development of therapeutic strategies. These include studies on the role of the epithelial Na+ channel ENaC, the development of the ENaC-overexpressing mouse as the first animal model with CF-like lung disease, and studies of functional consequences and pharmacological modulation of a large spectrum of CFTR mutations in model systems and patients with CF. The results of these studies contributed to the development of mucolytic and anti-inflammatory strategies, as well as emerging CFTR modulator therapies for CF. More recently, the Mall lab has focussed on the alternative epithelial Cl- conductance SLC26A9 as disease modifier and potential mutation-agnostic therapeutic target, the role of membrane-bound protease activity on airway neutrophils in structural lung damage, and the role of altered microbiota in CF airway inflammation.

Findings and novel therapeutic targets identified in experimental model systems are tested in observational studies and investigator-initiated clinical trials to accelerate the development of more effective therapies for patients with CF. In addition, the Mall lab has started to explore how results obtained from CF may be leveraged to improve our understanding of other severe progressive lung diseases such as primary ciliary dyskinesia (PCD) and interstitial lung diseases in children (chILD).

Team

Prof. Dr. med. Marcus A. Mall, Gruppenleiter (marcus.mall@charite.de)

Dr. sc. hum. Julia Gräber-Dürr, Laborleitung (julia.duerr@charite.de)
Dr. rer. nat. Nora Kofoed-Branzk, Wiss. Projektmanagement (nora.branzk@charite.de)

Dr. med. Simon Gräber, Clinician Scientist

Dr. rer. nat. Annalisa Addante, Postdoktorandin
Dr. med. Anita Balázs, Postdoktorandin
Dr. rer. nat. Constanze Vitzthum, Postdoktorandin
Dr. rer. nat. Markus Bardua, Postdoktorand

Dipl. Biol. Marika Drescher, Technische Assistenz
Dr. med. Maria Daniltchenko, Technische Assistenz
Diol. Ing. Alexander Rohrbach, Technische Assistenz 

Aktuelle Projekte

Regulation and pharmacological modulation of epithelial ion transport, airway surface liquid and mucociliary clearance in health and cystic fibrosis lung disease

Role of the Cl- transporter SLC26A9 as therapeutic target in cystic fibrosis

Role of surface-bound protease activity in cystic fibrosis airway inflammation and lung damage

Therapeutic targeting of altered airway microbiota to prevent airway inflammation and lung

Publikationen