Our research organization helps to discover new targets for therapeutic intervention in asthma by investigating possible primary alterations of the bronchial epithelium and their relative contribution to the pathogenesis of airway inflammation and defective tissue repair.
Studies conducted by our research team have revealed substantial differences between the asthmatic and normal epithelial cells in terms of permeability to antigens and ability to release growth factors and cytokines with proinflammatory activity constitutively or upon stimulation. The functional alterations of asthmatic epithelium likely reflect an intrinsic susceptibiliy to injury and may explain the reactive thickeness of the lamina reticularis that occurs at an early stage of the disease, even in absence of an evident inflammatory infiltrate.
We have recently identified a signaling pathway that normally regulates the epithelial response to stress and does not work effectively in the asthmatic epithelium. This altered response may make the asthmatic epithelium more susceptible than normal epithelium to the deleterious effects of mechanical or chemical stimuli and may lead to a progressive weakening of the epithelial barrier. The possibility that it may represent a novel therapeutic target is being evaluated in vitro and in vivo, by using in-house developed bio-engineered asthmatic bronchial tissue equivalents and appropriate animal models.
