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Long Term Chronic Pseudomonas aeruginosa Airway Infection in Mice
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Long Term Chronic Pseudomonas aeruginosa Airway Infection in Mice

Published on: March 17, 2014

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Particulate matter exposure promotes Pseudomonas aeruginosa invasion into airway epithelia by upregulating PAFR via

Jinguo Liu1, Xiaoyan Chen1, Jian Zhou1

  • 1Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University and Shanghai Respiratory Research Institute, 180 Fenglin Road, Shanghai, 200032, People's Republic of China.

Human Cell
|July 7, 2020
PubMed

Insights

Particulate matter (PM) exposure boosts Pseudomonas aeruginosa invasion into airway cells by increasing PAFR expression and activating the PI3K pathway. This finding offers new strategies against P. aeruginosa infections.

Area of Science:

  • * Environmental Health
  • * Microbiology
  • * Cell Biology

Background:

  • * Particulate matter (PM) exposure is linked to respiratory infections.
  • * Pseudomonas aeruginosa (P. aeruginosa) is a common respiratory pathogen.
  • * The interaction between PM exposure and P. aeruginosa invasion is not fully understood.

Purpose of the Study:

  • * To determine if PM exposure enhances P. aeruginosa invasion into airway epithelia.
  • * To elucidate the underlying molecular mechanisms of PM-induced P. aeruginosa invasion.
  • * To investigate the role of ROS, PI3K, and PAFR in this process.

Main Methods:

  • * Utilized human bronchial epithelial cells (BEAS-2B) and PAFR siRNA-transfected cells.
  • * Exposed cells to PM and treated with inhibitors (NAC, LY294002, BAY 11-7082, CV-3988).
  • * Assessed P. aeruginosa invasion via CFU assays and confocal microscopy; analyzed gene/protein expression using RT-PCR, immunofluorescence, flow cytometry, and Western blotting.

Main Results:

  • * PM exposure significantly promoted P. aeruginosa invasion through a ROS-dependent PI3K pathway, upregulating PAFR.
  • * NAC, PI3K inhibitor, and NF-κB inhibitor treatments alleviated PM-induced invasion.
  • * PAFR siRNA and antagonist treatments reduced PM-stimulated PI3K pathway activation and P. aeruginosa invasion.

Conclusions:

  • * PM exposure increases PAFR expression and activates the PI3K pathway in a ROS-dependent manner.
  • * A positive feedback loop between upregulated PAFR and activated PI3K promotes P. aeruginosa invasion.
  • * Targeting these mechanisms may offer novel therapeutic strategies against P. aeruginosa infections.
Keywords:
Oxidative stressParticulate matterPlatelet-activating factor receptorPseudomonas aeruginosa

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