CFTR Protects against Mycobacterium abscessus Infection by Fine-Tuning Host Oxidative Defenses

Abstract

Bernut et al. investigate the mechanism by which cystic fibrosis patients are vulnerable to Mycobacterium abscessus infection. Using zebrafish, they show that dysfunction of CFTR reduces both macrophage bactericidal activity and neutrophil recruitment to the forming protective granulomas. Together, this leads to hypersusceptibility to M. abscessus infection and larval death.