Tracking the immunopathological response to Pseudomonas aeruginosa during respiratory infections

• DOI: 10.1038/srep21465
• Publication Date: 2016-02-17T11:06:47Z
• Authors: Cristina Cigana; Nicola Ivan Lorè; Camilla Riva; Ida De Fino; Lorenza Spagnuolo; Barbara Sipione; Giacomo Rossi; Alessandro Nonis; Giulio Cabrini; Alessandra Bragonzi
• Keywords: Mice, Knockout; 0303 health sciences; Cystic Fibrosis; Animals; Cell Line; Chemokines; Cystic Fibrosis; Cytokines; Disease Models, Animal; Humans; Mice; Mice, Knockout; Opportunistic Infections; Pseudomonas Infections; Pseudomonas aeruginosa; Respiratory Tract Infections; Opportunistic Infections; Article; Cell Line; 3. Good health; Disease Models, Animal; Mice; 03 medical and health sciences; Pseudomonas aeruginosa; Animals; Cytokines; Humans; Pseudomonas Infections; Chemokines; Respiratory Tract Infections

Abstract Repeated cycles of infections, caused mainly by Pseudomonas aeruginosa, combined with a robust host immune response and tissue injury, determine the course outcome cystic fibrosis (CF) lung disease. As disease progresses, P. aeruginosa adapts to modifying dramatically its phenotype; however, it remains unclear whether how bacterial adaptive variants their persistence influence pathogenesis development. Using in vitro murine models infection, we showed that CF-adaptive shaped innate favoring persistence. Next, refined model chronic pneumonia extending infection up three months. In this model, including CFTR-deficient mice, unveil lead CF hallmarks airway remodelling fibrosis, epithelial hyperplasia structure degeneration, goblet cell metaplasia, collagen deposition, elastin degradation several additional markers damage. This reproducing pathology, will be instrumental identify novel molecular targets test newly tailored molecules inhibiting inflammation damage processes pre-clinical studies.