Asthma is a chronic, autoimmune, pulmonary disease characterized by airway inflammation, reversible airway obstruction and increased responsiveness to a variety of environmental stimuli.   T-cell activation of the allergic response is a key event in the inflammation that characterizes asthma as T-cells’ secretory products, cytokines, perpetuate airway inflammation.  Cytokines produced by CD4Th2 T-cells, including IL-4 and Il-5, promote growth and differentiation of inflammatory cells, activate them and induce their migration into the airways, and prolong their survival.

In the US, between 1980 and 2002 the number of Americans with asthma almost tripled reaching close to 20 million, and with the continuing steady rise in prevalence, this constitutes an epidemic.   Even if growth in prevalence were to stabilize, asthma will continue to constitute a tremendous healthcare burden and public health problem, responsible for 10 million doctor visits per year, 2.0 million emergency room visits per year and ½ million hospitalizations per year.   The prevailing consensus for this dramatic increase is attributed to the westernization of society and environmental factors.

As in many autoimmune diseases including celiac disease, barrier function in asthma patients is compromised.   Tight junctions of the epithelial cellular barrier in the lungs of asthma patients are leaky.  This loss of barrier function allows antigens and environmental triggers to pass through the epithelial barrier and elicit a T-cell mediated autoimmune response in genetically susceptible individuals.  Alba’s approach to therapeutic intervention for asthma focuses on barrier function and the inhibition of increased paracellular permeability leading to the increased presentation of environmental stimuli and, ultimately, the inflammatory cascade.