After obtaining her PhD in 1993 at the University of Nice, France, she spent 4 years as a post-doctoral fellow at University College Cork funded by the Cystic Fibrosis Association of Ireland and by the French CF Association. In 1998, she obtained a Wellcome Trust Project grant on “the autocrine role of CFTR”. This work led on to the award of a Wellcome Trust Advanced Fellowship which allowed her to return to France, in Montpellier. In 2003, she was successful for a permanent appointment as a researcher of the French National Institute of Health, INSERM, where she has continued to work in the area of CF and lung disease. She developed other studies on airway epithelial functions and obtained funding for translational studies on the regulation of airway epithelial secretory functions.
Using electrophysiology techniques (patch-clamp, Ussing chambers) and confocal microscopy techniques, her research has revealed novel effects of the endogenous lipoxin, LXA4 on airway epithelium function in addition to its known anti-inflammatory actions. Dr Urbach has chosen to expand this lipoxin project into paediatric CF studies at the National Children Research Centre at Crumlin Hospital in Dublin. Dr Urbach has obtained a 3 year leave-of-absence from INSERM to pursue this project at the NCRC with an honorary lecturer appointment at RCSI under a collaboration agreement in Translational Research between RCSI-INSERM-CNRS-University of Montpellier signed in the Irish Embassy Paris, January 2009.
Physiological impact of lipoxins on the function of lung epithelium from children with cystic fibrosis.
Cystic Fibrosis (CF) is the most common lethal genetic disease among Caucasians, and is characterised by progressive lung damage leading to early death. In healthy individuals, the body secretes a thin layer of fluid, which lines the airways and helps to fight infection by clearing mucus. The volume and composition of this fluid is tightly controlled. The gene mutation in CF leads to abnormal salt and water levels in this fluid, adversely affecting its protective functions. This leads to difficulty in clearing infection from the lungs with resultant infection and inflammation – the cause of lung damage over time. A lipid molecule, called lipoxin and produced in healthy lungs to fight inflammation has been shown to be low in individuals with CF. Little is known about how this important molecule affects CF airway cells and the airway fluid layer.
This research program is based on the hypothesis that the endogenous lipoxin, LXA4, exerts beneficial effects on airway epithelial function in CF through enhanced mucociliary clearance and epithelial repair. This project is focused on the actions of LXA4 on six major physiological functions controlled by the airway epithelium and which are altered in CF: (i) Cl- secretion, (ii) Na+ absorption, (iii) ASL height, (iv) ciliary beat frequency, (v) airway epithelial repair and (vi) tight junction formation. The project uses a range of molecular biology, electrophysiological and advanced imaging technologies applied to CF and non-CF airway epithelial primary cultures grown from biopsies in children and non-CF (Nuli-1) and CF Phe508del (CuFi-1) human cell lines.
Since airway epithelial cells can be targeted by inhaled nebulised LXA4 and its stable analogues, this work has the potential to open up innovative therapy in CF.