Scientific article
Open access

Vav3 mediates pseudomonas aeruginosa adhesion to the cystic fibrosis airway epithelium

Published inCell Reports, vol. 32, no. 1, 107842
Publication date2020

Pseudomonas aeruginosa (Pa) represents the leading cause of airway infection in cystic fibrosis (CF). Early airways colonization can be explained by enhanced adhesion of Pa to the respiratory epithelium. RNA sequencing (RNA-seq) on fully differentiated primary cultures of airway epithelial cells from CF and non-CF donors predict that VAV3, β1 INTEGRIN, and FIBRONECTIN genes are significantly enriched in CF. Indeed, Vav3 is apically overexpressed in CF, associates with active β1 integrin luminally exposed, and increases fibronectin deposition. These luminal microdomains, rich in fibronectin and β1 integrin and regulated by Vav3, mediate the increased Pa adhesion to the CF epithelium. Interestingly, Vav3 inhibition normalizes the CF-dependent fibronectin and β1-integrin ectopic expression, improves the CF epithelial integrity, and prevents the enhanced Pa trapping to the CF epithelium. Through its capacity to promote a luminal complex with active β1 integrin and fibronectin that favors bacteria trapping, Vav3 may represent a new target in CF.

  • Pseudomonas aeruginosa
  • Rho-GTPases
  • Vav3
  • Airway epithelial cells
  • Cystic fibrosis
  • Fibronectin
  • Guanine exchange factors
  • Host-pathogen interaction
  • Β1 integrin
Citation (ISO format)
BADAOUI, Mehdi et al. Vav3 mediates pseudomonas aeruginosa adhesion to the cystic fibrosis airway epithelium. In: Cell Reports, 2020, vol. 32, n° 1, p. 107842. doi: 10.1016/j.celrep.2020.107842
Main files (1)
Article (Published version)
Secondary files (1)
ISSN of the journal2211-1247

Technical informations

Creation07/14/2020 9:59:00 AM
First validation07/14/2020 9:59:00 AM
Update time03/15/2023 10:24:04 PM
Status update03/15/2023 10:24:03 PM
Last indexation08/30/2023 11:17:42 PM
All rights reserved by Archive ouverte UNIGE and the University of GenevaunigeBlack