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Cell Host Microbe. 2019 Jan 9;25(1):140-152.e6. doi: 10.1016/j.chom.2018.11.008. Epub 2018 Dec 20.

A Surface-Induced Asymmetric Program Promotes Tissue Colonization by Pseudomonas aeruginosa.

Author information

1
Focal Area Infection Biology, Biozentrum, University of Basel, Basel, Switzerland.
2
IPBS - UMR 5089, Toulouse, France.
3
Department of Biochemistry, University of Lausanne, Lausanne, Switzerland.
4
Focal Area Infection Biology, Biozentrum, University of Basel, Basel, Switzerland. Electronic address: urs.jenal@unibas.ch.

Abstract

The opportunistic human pathogen Pseudomonas aeruginosa effectively colonizes host epithelia using pili as primary adhesins. Here we uncover a surface-specific asymmetric virulence program that enhances P. aeruginosa host colonization. We show that when P. aeruginosa encounters surfaces, the concentration of the second messenger c-di-GMP increases within a few seconds. This leads to surface adherence and virulence induction by stimulating pili assembly through activation of the c-di-GMP receptor FimW. Surface-attached bacteria divide asymmetrically to generate a piliated, surface-committed progeny (striker) and a flagellated, motile offspring that leaves the surface to colonize distant sites (spreader). Cell differentiation is driven by a phosphodiesterase that asymmetrically positions to the flagellated pole, thereby maintaining c-di-GMP levels low in the motile offspring. Infection experiments demonstrate that cellular asymmetry strongly boosts infection spread and tissue damage. Thus, P. aeruginosa promotes surface colonization and infection transmission through a cooperative virulence program that we termed Touch-Seed-and-Go.

KEYWORDS:

Pseudomonas aeruginosa; asymmetric division; c-di-GMP; flagella; second messenger; surface sensing; tissue colonization; type IV pili; virulence

PMID:
30581112
DOI:
10.1016/j.chom.2018.11.008

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