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Host cell surfaces induce a Type IV pili-dependent alteration of bacterial swimming.

ABSTRACT: For most pathogenic bacteria, flagellar motility is recognized as a virulence factor. Here, we analysed the swimming behaviour of bacteria close to eukaryotic cellular surfaces, using the major opportunistic pathogen Pseudomonas aeruginosa as a model. We delineated three classes of swimming trajectories on both cellular surfaces and glass that could be differentiated by their speeds and local curvatures, resulting from different levels of hydrodynamic interactions with the surface. Segmentation of the trajectories into linear and curved sections or pause allowed us to precisely describe the corresponding swimming patterns near the two surfaces. We concluded that (i) the trajectory classes were of same nature on cells and glass, however the trajectory distribution was strikingly different between surface types, (ii) on cell monolayers, a larger fraction of bacteria adopted a swimming mode with stronger bacteria-surface interaction mostly dependent upon Type IV pili. Thus, bacteria swim near boundaries with diverse patterns and importantly, Type IV pili differentially influence swimming near cellular and abiotic surfaces.

SUBMITTER: Golovkine G

PROVIDER: S-EPMC5155295 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature

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Host cell surfaces induce a Type IV pili-dependent alteration of bacterial swimming.

Golovkine Guillaume G Lemelle Laurence L Burny Claire C Vaillant Cedric C Palierne Jean-Francois JF Place Christophe C Huber Philippe P

Scientific reports 20161214

For most pathogenic bacteria, flagellar motility is recognized as a virulence factor. Here, we analysed the swimming behaviour of bacteria close to eukaryotic cellular surfaces, using the major opportunistic pathogen Pseudomonas aeruginosa as a model. We delineated three classes of swimming trajectories on both cellular surfaces and glass that could be differentiated by their speeds and local curvatures, resulting from different levels of hydrodynamic interactions with the surface. Segmentation ...[more]

PMID: 27966607

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Project description:Neisseria meningitidis is a strictly human pathogen that has two facets since asymptomatic carriage can unpredictably turn into fulminant forms of infection. Meningococcal pathogenesis relies on the ability of the bacteria to break host epithelial or endothelial cellular barriers. Highly restrictive, yet poorly understood, mechanisms allow meningococcal adhesion to cells of only human origin. Adhesion of encapsulated and virulent meningococci to human cells relies on the expression of bacterial type four pili (T4P) that trigger intense host cell signalling. Among the components of the meningococcal T4P, the concomitantly expressed PilC1 and PilC2 proteins regulate pili exposure at the bacterial surface, and until now, PilC1 was believed to be specifically responsible for T4P-mediated meningococcal adhesion to human cells. Contrary to previous reports, we show that, like PilC1, the meningococcal PilC2 component is capable of mediating adhesion to human ME180 epithelial cells, with cortical plaque formation and F-actin condensation. However, PilC1 and PilC2 promote different effects on infected cells. Cellular tracking analysis revealed that PilC1-expressing meningococci caused a severe reduction in the motility of infected cells, which was not the case when cells were infected with PilC2-expressing strains. The amount of both total and phosphorylated forms of EGFR was dramatically reduced in cells upon PilC1-mediated infection. In contrast, PilC2-mediated infection did not notably affect the EGFR pathway, and these specificities were shared among unrelated meningococcal strains. These results suggest that meningococci have evolved a highly discriminative tool for differential adhesion in specific microenvironments where different cell types are present. Moreover, the fine-tuning of cellular control through the combined action of two concomitantly expressed, but distinctly regulated, T4P-associated variants of the same molecule (i.e. PilC1 and PilC2) brings a new model to light for the analysis of the interplay between pathogenic bacteria and human host cells.

Dataset Information

Host cell surfaces induce a Type IV pili-dependent alteration of bacterial swimming.

Publications

Host cell surfaces induce a Type IV pili-dependent alteration of bacterial swimming.

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