Last month the lead article in the New England Journal of Medicine was titled “A Large-Scale, Consortium-Based Genome-Wide Association Study of Asthma”, and was from work done by the National Heart and Lung Institute in the U.K.

It was a detailed, in-depth study that led to two major findings: First, asthma is genetically heterogenous.  This fact accounts for the variability in the illness itself, and also to the variability in response to treatments.  That is, when an inhaler that works beautifully in one asthmatic fails to help a second person, the reason may well be that they have two different asthmatic illnesses based on genetics.

On thing in common for all the asthma genes is that they all seem to lead to a defect in the epithelial barrier of the airways.  This faulty barrier leads to damage from the adaptive immune system, and the resultant airway inflammation.  Reason?  Because viruses, bacteria and allergens can more easily invade these porous airways.

The second finding was that elevated levels of IgE are not the seminal cause for asthma, but rather occur in response to this airway porosity with resultant greater exposure to allergens.

Still, this finding does not negate the fact that therapies directed at elevated IgE are exceedingly helpful in treating asthma.

This research will lead to greater efforts at altering gene defects, and also at means to improve the airway epithelail barrier function.