During acute infection,
P. aeruginosa can translocate to the blood compartment and disseminate to secondary infected organs. In preliminary steps, bacteria can use flagellar motility to generate three types of trajectories close to host cell monolayers that can be useful either to scan mucosae for transmigration opportunities or for large-scale investigations
[4]. Bacteria can form aggregates at the surface of epithelial monolayers, but only individual swimming bacteria can transmigrate. Transmigration occurs at cell-cell junctions, exploiting sites of cell division and senescent cell extrusion. For transmigration, bacteria need a flagellum, type IV pili and a functional T3SS
[5]. Transmigration across endothelial monolayers is faster, as VE-cadherin, the major adhesive protein located at interendothelial junctions, is cleaved by LasB, a protease secreted by
P. aeruginosa’s T2SS
[6].
Confocal images in (x,y), (x,z) and (y,z) showing the transmigration of bacteria (red) in a cleft (arrowhead) formed between two dividing MDCK cells (*). Scale bar: 20 μm.
Golovkine G.
et al (2016)
PLoS Pathog [5]
Confocal images in (x,y) and (x,z) showing a bacterial penetration (arrowhead) at intercellular junctions at site of senescent cell extrusion (*). Scale bar: 15 μm.
Golovkine G.
et al (2016)
PLoS Pathog [5]
References[4] Golovkine
et al (2016)
Scientific reports 6:38950
[5] Golovkine
et al (2016)
PLoS pathogens 12(1):e1005377
[6] Golovkine
et al (2014)
PLoS pathogens 10(3):e1003939.