Pseudomonas pyocyanine alters calcium signaling in human airway epithelial cells

Gerene M. Denning, Michelle A. Railsback, George T. Rasmussen, Charles D. Cox, Bradley E. Britigan

Research output: Contribution to journalArticlepeer-review

70 Scopus citations

Abstract

Pseudomonas aeruginosa, an opportunistic human pathogen, causes both acute and chronic lung disease. P. aeruginosa exerts many of its pathophysiological effects by secreting virulence factors, including pyocyanine, a redox-active compound that increases intracellular oxidant stress. Because oxidant stress has been shown to affect cytosolic Ca2+ concentration ([Ca2+](c)) in other cell types, we studied the effect of pyocyanine on [Ca2+](c) in human airway epithelial cells (A549 and HBE). At lower concentrations, pyocyanine inhibits inositol 1,4,5-trisphosphate formation and [Ca2+](c) increases in response to G protein-coupled receptor agonists. Conversely, at higher concentrations, pyocyanine itself increases [Ca2+](c). The pyocyanine-dependent [Ca2+](c) increase appears to be oxidant dependent and to result from increased inositol trisphosphate and release of Ca2+ from intracellular stores. Ca2+ plays a central role in epithelial cell function, including regulation of ion transport, mucus secretion, and ciliary beat frequency. By disrupting Ca2+ homeostasis, pyocyanine could interfere with these critical functions and contribute to the pathophysiological effects observed in Pseudomonas-associated lung disease.

Original languageEnglish (US)
Pages (from-to)L893-L900
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume274
Issue number6 18-6
DOIs
StatePublished - Jun 1998
Externally publishedYes

Keywords

  • A549 cells
  • G protein-coupled receptors
  • HBE cells
  • Inositol phosphates
  • Oxidants

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology

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