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Neuropeptides and capsaicin stimulate the release of inflammatory cytokines in a human bronchial epithelial cell line.

Publication ,  Journal Article
Veronesi, B; Carter, JD; Devlin, RB; Simon, SA; Oortgiesen, M
Published in: Neuropeptides
December 1999

The role of neuropeptides in initiating and modulating airway inflammation was examined in a human bronchial epithelial cell line (i.e. BEAS-2B). At a range of concentrations, exposure of BEAS-2B cells to Substance P (SP) or calcitonin gene related protein resulted in immediate increases in intracellular calcium ([Ca(2+)](i)), the synthesis of the transcripts for the inflammatory cytokines, IL-6, IL-8 and TNFalpha after 2 h exposure, and the release of their proteins after 6 h exposure. Addition of thiorphan (100 nM), an inhibitor of neutral endopeptidase, enhanced the levels of SP-stimulated cytokine release. Stimulation of IL-6 by SP occurred in a conventional receptor-mediated manner as demonstrated by its differential release by fragments SP 4-11 and SP 1-4 and by the blockage of IL-6 release with the non-peptide, NK-1 receptor antagonist, CP-99 994. In addition to the direct stimulation of inflammatory cytokines, SP (0.5 microM), in combination with TNFalpha (25 units/ml), synergistically stimulated IL-6 release. BEAS-2B cells also responded to the botanical irritant, capsaicin (10 microM) with increases in [Ca(2+)](i) and IL-8 cytokine release after 4 h exposure. The IL-8 release was dependent on the presence of extracellular calcium. Capsaicin-stimulated increases of [Ca(2+)](i) and cytokine release could be reduced to control levels by pre-exposure to capsazepine, an antagonist of capsaicin (i.e. vanilloid) receptor(s) or by deletion of extracellular calcium from the exposure media. The present data indicate that the BEAS-2B human epithelial cell line expresses neuropeptide and capsaicin-sensitive pathways, whose activation results in immediate increases of [Ca(2+)](i) stimulation of inflammatory cytokine transcripts and the release of their cytokine proteins.

Duke Scholars

Published In

Neuropeptides

DOI

ISSN

0143-4179

Publication Date

December 1999

Volume

33

Issue

6

Start / End Page

447 / 456

Location

Netherlands

Related Subject Headings

  • Tumor Necrosis Factor-alpha
  • Thiorphan
  • Substance P
  • RNA, Messenger
  • Protease Inhibitors
  • Piperidines
  • Peptide Fragments
  • Neurology & Neurosurgery
  • Interleukin-8
  • Interleukin-6
 

Citation

APA
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ICMJE
MLA
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Veronesi, B., Carter, J. D., Devlin, R. B., Simon, S. A., & Oortgiesen, M. (1999). Neuropeptides and capsaicin stimulate the release of inflammatory cytokines in a human bronchial epithelial cell line. Neuropeptides, 33(6), 447–456. https://doi.org/10.1054/npep.1999.0761
Veronesi, B., J. D. Carter, R. B. Devlin, S. A. Simon, and M. Oortgiesen. “Neuropeptides and capsaicin stimulate the release of inflammatory cytokines in a human bronchial epithelial cell line.Neuropeptides 33, no. 6 (December 1999): 447–56. https://doi.org/10.1054/npep.1999.0761.
Veronesi B, Carter JD, Devlin RB, Simon SA, Oortgiesen M. Neuropeptides and capsaicin stimulate the release of inflammatory cytokines in a human bronchial epithelial cell line. Neuropeptides. 1999 Dec;33(6):447–56.
Veronesi, B., et al. “Neuropeptides and capsaicin stimulate the release of inflammatory cytokines in a human bronchial epithelial cell line.Neuropeptides, vol. 33, no. 6, Dec. 1999, pp. 447–56. Pubmed, doi:10.1054/npep.1999.0761.
Veronesi B, Carter JD, Devlin RB, Simon SA, Oortgiesen M. Neuropeptides and capsaicin stimulate the release of inflammatory cytokines in a human bronchial epithelial cell line. Neuropeptides. 1999 Dec;33(6):447–456.
Journal cover image

Published In

Neuropeptides

DOI

ISSN

0143-4179

Publication Date

December 1999

Volume

33

Issue

6

Start / End Page

447 / 456

Location

Netherlands

Related Subject Headings

  • Tumor Necrosis Factor-alpha
  • Thiorphan
  • Substance P
  • RNA, Messenger
  • Protease Inhibitors
  • Piperidines
  • Peptide Fragments
  • Neurology & Neurosurgery
  • Interleukin-8
  • Interleukin-6