Wound-healing peptides curb bacterial colonization in cystic fibrosis airway models

Cystic fibrosis, one of the most common genetic diseases in Switzerland, promotes chronic bacterial infections by impairing the protective barrier of the airways. Scientists at the University of Geneva (UNIGE) have discovered that this dysfunction is caused by the abnormal activation of a protein, connexin 43, which disrupts cellular organization and compromises the integrity of the airways.

The team has not only shed light on this molecular mechanism using 3D models of cells derived from human lungs but has also succeeded in correcting the defect using molecules already undergoing clinical trials in dermatology and oncology. Preventing pathogenic bacteria from attaching to the airways of people with cystic fibrosis could therefore help limit serious complications.

These findings are published in the journal Communications Biology.

Despite significant therapeutic advances, chronic pulmonary infections persist in many patients with cystic fibrosis. Eradicating respiratory pathogens therefore remains a major challenge.

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