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Methods for Detecting Cytotoxic Amyloids Following Infection of Pulmonary Endothelial Cells by Pseudomonas aeruginosa
07:27

Methods for Detecting Cytotoxic Amyloids Following Infection of Pulmonary Endothelial Cells by Pseudomonas aeruginosa

Published on: July 12, 2018

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Virulent Pseudomonas aeruginosa infection converts antimicrobial amyloids into cytotoxic prions

Sarah Voth1,2, Meredith Gwin1,2, Christopher Michael Francis1,2

  • 1Department of Physiology and Cell Biology, College of Medicine, University of South Alabama, Mobile, AL, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|May 16, 2020
PubMed

Insights

Pseudomonas aeruginosa infection triggers cytotoxic amyloids from lung cells. The type III secretion system, particularly exoenzyme Y, drives this process, potentially creating a prion-like strain and impacting host defense.

Area of Science:

  • Microbiology
  • Cell Biology
  • Immunology

Background:

  • Pseudomonas aeruginosa infections can lead to cytotoxic amyloid production in lung endothelium.
  • The precise molecular mechanisms governing this host-pathogen interaction and amyloidogenesis remain unclear.

Purpose of the Study:

  • To investigate the role of type III secretion system (T3SS) effectors in Pseudomonas aeruginosa-induced cytotoxic amyloid production.
  • To elucidate the contribution of specific T3SS effectors, such as exoenzyme Y (ExoY), in amyloid virulence and propagation.

Main Methods:

  • Examined the impact of T3SS-proficient and T3SS-deficient Pseudomonas aeruginosa strains on lung endothelial cells.
  • Utilized various T3SS effector combinations, including ExoY, ExoS, and T, to induce amyloid production.
  • Assessed the cytotoxic and propagation characteristics of induced amyloids in endothelial cell cultures.

Main Results:

  • A functional T3SS and its effectors in P. aeruginosa induced cytotoxic amyloids (including beta-amyloid and tau) from lung endothelium.
  • Intoxication with ExoY, alone or with ExoS/T, resulted in the most virulent amyloids, capable of prion-like propagation.
  • T3SS-incompetent P. aeruginosa produced non-cytotoxic, antimicrobial amyloids.

Conclusions:

  • Endothelial intoxication by ExoY is sufficient to trigger self-propagating amyloid cytotoxins during P. aeruginosa infection.
  • Pulmonary endothelium plays a role in innate immunity by producing antimicrobial amyloids in response to infection.
  • ExoY contributes to P. aeruginosa virulence by subverting endothelial amyloid host defense, leading to cytotoxic proteinopathy.
Keywords:
amyloid beta (Aβ)exoenzyme Y (ExoY)nosocomial pneumoniapriontau (τ)

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