Asthma is a disease of civilisation par excellence. Its increasing incidence is cause for concern and several teams working around the world are attempting to untangle the complexity of its causes. The University of Liège has made a small step towards this understanding by identifying a protease whose role may prove to be very interesting ...

Asthma may be defined as a reversible obstruction of the bronchial tubes, resulting in inflammation. The cause of this is most often allergen exposure. Although the general public is aware of the classic image of an asthma attack - wheezing, breathlessness and respiratory distress - researchers are more interested in what happens between attacks.  This is because they consider asthma as a chronic illness, with the attack being a particularly acute - and distressing - manifestation of a more global pathological process taking place in the depths of the bronchial tree.

Asthma's characteristic narrowing of the internal diameter of the bronchial tubes results from the combination of hyperactivity of the smooth muscles that surround the airways and the hypersecretion of mucous by the glands coating the inner walls. These two elements are caused by a persistent inflammatory reaction. It is the cause of this reaction that is of interest to researchers. It is probably due to environmental factors which may themselves be allergens or may be simply irritating agents (atmospheric pollution for example). However, not everyone becomes asthmatic even when people are allergic or breathe polluted air. And in contrast, in asthmatic families, some individuals suffer from the illness while others don't. There is therefore an individual predisposition involved, which is genetic in nature.

'The problem is that this is not a mutation of a specific gene as in the case of cystic fibrosis, says Professor Didier Cataldo, lung specialist at the Sart Tilman CHU and lecturer at  ULg. In asthma, there are probably at least two dozen genes involved. This explains why people can be asthmatic for very different reasons. Classically, an asthmatic child generally has an allergic profile that may have started with cradle cap at two months, followed by eczema in infancy. The first signs of asthma often appear during infections by minor respiratory viruses which are inevitable in children, and some young asthmatics have steroid inhalers from a young age. Later, the symptoms may abate or may last throughout their lives. However, there are also people who develop asthma following acute exposure to chlorine gas, in the working environment, for example. This purely chemical, irritative asthma, can be found in swimming pool technicians. Other forms, often fairly severe, develop later; patients for whom classical treatment generally is not effective. Asthma is therefore a highly polymorphic syndrome that covers a range of what are probably different molecular and physio-pathological mechanisms. Obviously, this explains why it is difficult to find 'the' gene. We thus feel disempowered, because we can't offer patients a genetic analysis to determine their likelihood of developing asthma. ' (see also the articles Asthma, a very mysterious disease and Turning asthma on its head)