์ฝ˜ํ…์ธ ๋กœ ๊ฑด๋„ˆ๋›ฐ๊ธฐ
Merck

Vav3 Mediates Pseudomonas aeruginosa Adhesion to the Cystic Fibrosis Airway Epithelium.

Cell reports (2020-07-09)
Mehdi Badaoui, Alice Zoso, Tahir Idris, Marc Bacchetta, Juliette Simonin, Sylvain Lemeille, Bernhard Wehrle-Haller, Marc Chanson
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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, ฮฒ1 INTEGRIN, and FIBRONECTIN genes are significantly enriched in CF. Indeed, Vav3 is apically overexpressed in CF, associates with active ฮฒ1 integrin luminally exposed, and increases fibronectin deposition. These luminal microdomains, rich in fibronectin and ฮฒ1 integrin and regulated by Vav3, mediate the increased Pa adhesion to the CF epithelium. Interestingly, Vav3 inhibition normalizes the CF-dependent fibronectin and ฮฒ1-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 ฮฒ1 integrin and fibronectin that favors bacteria trapping, Vav3 may represent a new target in CF.

MATERIALS
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Sigma-Aldrich
Anti-Vav3 Antibody, human, Upstateยฎ, from rabbit
Sigma-Aldrich
Anti-Glyceraldehyde-3-Phosphate Dehydrogenase Antibody, clone 6C5, clone 6C5, Chemiconยฎ, from mouse