Benoît-Joseph Laventie

Abstract Transwell-based airway models have become increasingly important to study the effects of respiratory diseases and drug treatment at the air-liquid interface of the lung epithelial barrier. However, the underlying mechanisms at tissue and cell level often remain unclear, as transwell inserts feature limited live-cell imaging compatibility.

Abstract Efficient colonization of mucosal surfaces is essential for opportunistic pathogens like Pseudomonas aeruginosa, but how bacteria collectively and individually adapt to optimize adherence, virulence and dispersal is largely unclear. Here we identified a stochastic genetic switch, hecR–hecE, which is expressed bimodally and generates functionally distinct bacterial subpopulations to balance P. aeruginosa growth and dispersal on surfaces.

Highlights • P. aeruginosa rapidly boosts c-di-GMP upon surface contact to activate adherent pili • Mechanosensation requires a functional flagellar motor to activate c-di-GMP receptors • Surface colonization triggers asymmetric division to generate specialized progeny • Asymmetric divisions promote infection spread and tissue damage Summary The opportunistic human pathogen Pseudomonas aeruginosa effectively colonizes host epithelia using pili as primary adhesins.