Cystic fibrosis is the most common genetic disease in Europe. It is caused by dysfunctions of the CFTR anion channel. In addition to regulating the output of chlorine, CFTR negatively regulates the activity of the sodium epithelial channel ENaC. In CF patients, at the epithelial level, CFTR dysfunction leads to intracellular chlorine accumulation and ENaC hyperactivity leading to uncontrolled sodium entry into the cells. Depending on the osmotic gradient, water enters the cells in a massive manner, causing dehydration of the mucus bordering the epithelium. This creates a favourable environment for the accumulation and growth of a number of pathogenic and opportunistic pathogens including Mycobacterium abscessus.
In people with cystic fibrosis, the prevalence of M. abscessus varies from 3 to 10% in France. In comparison, in healthy people, the prevalence of M. abscessus infections is around 1/100,000 per habitant.
With a Drosophila infection model with cystic fibrosis phenotype, we want to identify the host factors that favor M. abscessus infection in the context of cystic fibrosis.
