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Benzo(a)pyrene suppresses tracheal antimicrobial peptide gene expression in bovine tracheal epithelial cells.

Authors
  • Bourque, Laura A1
  • Raverty, Stephen2
  • Co, Carmon3
  • Lillie, Brandon N4
  • Daoust, Pierre-Yves5
  • Clark, Mary Ellen6
  • Caswell, Jeff L7
  • 1 Department of Pathobiology, University of Guelph, N1G 2W1 Guelph, ON, Canada; Canadian Wildlife Health Cooperative, Department of Pathology & Microbiology, Atlantic Veterinary College, University of Prince Edward Island, 550 University Avenue, C1A 4P3 Charlottetown, PE, Canada. Electronic address: [email protected] , (Canada)
  • 2 Animal Health Center, 1767 Angus Campbell Road, V3G 2M3 Abbotsford, BC, Canada. Electronic address: [email protected] , (Canada)
  • 3 Department of Pathobiology, University of Guelph, N1G 2W1 Guelph, ON, Canada. Electronic address: [email protected] , (Canada)
  • 4 Department of Pathobiology, University of Guelph, N1G 2W1 Guelph, ON, Canada. Electronic address: [email protected] , (Canada)
  • 5 Canadian Wildlife Health Cooperative, Department of Pathology & Microbiology, Atlantic Veterinary College, University of Prince Edward Island, 550 University Avenue, C1A 4P3 Charlottetown, PE, Canada. Electronic address: [email protected] , (Canada)
  • 6 Department of Pathobiology, University of Guelph, N1G 2W1 Guelph, ON, Canada. , (Canada)
  • 7 Department of Pathobiology, University of Guelph, N1G 2W1 Guelph, ON, Canada. Electronic address: [email protected] , (Canada)
Type
Published Article
Journal
Veterinary immunology and immunopathology
Publication Date
Sep 01, 2018
Volume
203
Pages
40–46
Identifiers
DOI: 10.1016/j.vetimm.2018.08.001
PMID: 30243371
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Respiratory disease is an important cause of morbidity and mortality in cetaceans, which are also threatened by environmental degradation caused by crude oil spills. Following oil spills, cetaceans at the water surface may inhale droplets of oil containing toxic polycyclic aromatic hydrocarbons (PAHs), which could potentially alter respiratory immunity via activation of the aryl hydrocarbon receptor (AHR) and its subsequent interaction with nuclear factor kappa B (NF-κB). β-defensins are antimicrobial peptides secreted by airway epithelial cells and their expression is known to be dependent on NF-κB. We hypothesized that PAHs may suppress the expression of β-defensins, and thereby contribute to the pathogenesis of pneumonia. This hypothesis was modeled by measuring the in vitro effects of benzo(a)pyrene (BAP), phenanthrene, and naphthalene on tracheal antimicrobial peptide (TAP) gene expression in bovine tracheal epithelial cells. Stimulation with lipopolysaccharide (LPS) induced 20 ± 17-fold (mean ± SD) increased TAP gene expression. Exposure of tracheal epithelial cells to 5 μM BAP for 4 or 8 h, followed by incubation with a combination of LPS and 5 μM BAP for another 16 h, significantly (P = 0.002) suppressed LPS-induced TAP gene expression by 40.6 ± 21.8% (mean ± SD) in tracheal epithelial cells from 9 calves tested. BAP-induced suppression of TAP gene expression coincided with induction of cytochrome P450 1A1 gene expression. In contrast, phenanthrene and naphthalene had no consistent effect, and exposure to PAHs did not significantly affect constitutive TAP gene expression (i.e. without LPS). These findings characterize the suppressive effects of BAP-a toxic pollutant found in crude oil-on this respiratory innate immune response. Copyright © 2018 Elsevier B.V. All rights reserved.

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