Alveolar ion and fluid transport are critically impaired in mechanically ventilated patients with acute lung injury (ALI), or in its severest form, acute respiratory distress syndrome (ARDS), leading to pulmonary oedema (see figure 1), and death.

This syndrome is responsible for a high proportion of patient deaths in the adult intensive care unit. Members of the Morty Laboratory investigate the mechanisms of how ions and water are normally transported into and out of the lung, and what happens when these mechanisms fail in patients with pulmonary oedema.

The studies are aiming to obtain a better understanding of the molecular mechanisms underlying the development of ARDS, and so establish better management strategies for patients with this devastating syndrome.

One of the aims of normal lung development is to maximise the total surface area available in the lung for gas exchange, and to reduce the distance between the blood circulation and the lung/air interface, to allow for effective transport of oxygen into the bloodstream, and carbon dioxide out of the bloodstream.

In humans, lung development proceeds until at least seven years of age, and possibly longer. How the lung is programmed to achieve this is currently unknown. Lung development is initiated with the separation of the primitive respiratory system from the gut and the branching of the bronchi (early lung development), and later, the development of the alveoli - the functional gas exchange units of the lung (late lung development). This process is illustrated schematically in figure 2.

Members of the Morty Laboratory are currently exploring the genetic mechanisms which drive the process of septation, where alveolar walls divide to generate large numbers of alveoli, as well as how blood vessels form and grow, to support the developmnet of the alveolar structures.

Late lung developmnet is dangerously impacted when infants are born prematurely. These infants are ventilated to support life (see figure 3). However, this ventilation process is very damaging to the lung and can cause bronchopulmonary dysplasia (BPD). In this case the alveolar structure is perturbed in affected patients, with consequences that extend into adulthood.

Members of the Morty Laboratory are currently exploring what goes wrong, when premature infants are ventilated and develop BPD, with the aim to develop new ways to clinically manage this complex and important clinical problem encountered in the neonatal intensive care unit.