Protection of lung cells from cigarette smoke, a primary insult causing chronic obstructive pulmonary disease (COPD) and other lung diseases, and ability to increase airway surface hydration and maintain ciliary function.

Unmet Need
Chronic obstructive pulmonary disease (COPD) is predicted to become the third leading cause of death globally by 2030, with cigarette smoke being a major cause. Despite the prevalence of COPD there has been very little progress in developing therapeutic strategy in past 20 years. Thus, mechanistic studies for therapeutic targets for treating COPD and other lung diseases is urgently needed.
 
Technology Overview
Johns Hopkins researchers have identified novel genes that protect lung cells from toxic insults such as cigarette smoke using a novel platform based upon Dictyostelium discoideum. One of the genes can maintain the metabolic state, the air surface liquid height and ciliary function in airway epithelium when exposed to insult like cigarette smoke. Further, the gene expression level is slightly reduced in patients with COPD and in the mouse model exposed to chronic cigarette smoke. Another protein also showed similar protection against cigarette smoke exposure. These genes could be used as pharmacological targets or as the basis of gene therapy strategy for treating COPD, asthma, cystic fibrosis and many other lung diseases.

Stage of Development
Discovery
 
Publications
None at this time.

Category(s):