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.
Cystic fibrosis, a prevalent genetic disease in Switzerland, generates persistent bacterial infections by compromising the airway's protective barrier. The University of Geneva's researchers have uncovered that this impairment is due to the abnormal activation of connexin 43, a protein responsible for cellular communication. 3D models of human lung cells revealed that excessive connexin 43 activity disrupts cell orientation and tissue organization, establishing anchor points for pathogenic bacteria to attach.
These anchor points are formed when connexin 43 is persistently active, even in healthy cells. The team found that mimetic peptides, similar to wound-healing molecules, can effectively reduce bacterial colonization by inhibiting connexin 43 activity. This discovery suggests that targeting connexin 43 regulation could provide an additional treatment option for cystic fibrosis patients suffering from chronic airway infections.
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