Researchers identify mechanism driving lung inflammation in cystic fibrosis

A study coordinated by the University of Milan and the National Research Council (CNR-IRGB) has identified a mechanism by which the bacterium Pseudomonas aeruginosa contributes to chronic lung inflammation in patients with cystic fibrosis.

Published in Nature Microbiology, the research demonstrates that the pathogen reprograms protective Th17 lymphocytes—which normally defend mucosal surfaces against infection—into pathogenic Th17 cells. These reprogrammed cells are capable of directly damaging the lung epithelium and triggering a persistent, unregulated inflammatory response.

Researchers observed an increase in two specific populations of pathogenic Th17 lymphocytes associated with Pseudomonas aeruginosa infections in cystic fibrosis lung samples. Notably, the study found that even bacterial strains isolated during the early stages of lung colonization are capable of promoting the generation of these pathogenic cells, suggesting a potential window for medical intervention before chronic inflammation becomes established.