Residual oil fly ash and charged polymers activate epithelial cells and nociceptive sensory neurons

Marga Oortgiesen*, Bellina Veronesi, Gary Eichenbaum, Patrick F. Kiser, Sidney A. Simon

*Corresponding author for this work

Research output: Contribution to journalArticle

38 Scopus citations

Abstract

Residual oil fly ash (ROFA) is an industrial pollutant that contains metals, acids, and unknown materials complexed to a particulate core. The heterogeneous composition of ROFA hampers finding the mechanism(s) by which it and other particulate pollutants cause airway toxicity. To distinguish culpable factors contributing to the effects of ROFA, synthetic polymer microsphere (SPM) analogs were synthesized that resembled ROFA in particle size (2 and 6 μm in diameter) and zeta potential (-29 mV). BEAS-2B human bronchial epithelial cells and dorsal root ganglion neurons responded to both ROFA and charged SPMs with an increase in intracellular Ca2+ concentration ([Ca2+](i)) and the release of the proinflammatory cytokine interleukin-6, whereas neutral SPMs bound with polyethylene glycol (0-Mv zeta potential) were relatively ineffective. In dorsal root ganglion neurons, the SPM-induced increases in [Ca2+](i) were correlated with the presence of acid- and/or capsaicin-sensitive pathways. We hypothesized that the acidic microenvironment associated with negatively charged colloids like ROFA and SPMs activate irritant receptors in airway target cells. This causes subsequent cytokine release, which mediates the pathophysiology of neurogenic airway inflammation.

Original languageEnglish (US)
Pages (from-to)L683-L695
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume278
Issue number4 22-4
StatePublished - Apr 1 2000

Keywords

  • Acid-sensitive receptors
  • Capsaicin receptors
  • Particulate matter
  • Zeta potential

ASJC Scopus subject areas

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

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