Next Article in Journal
Generation and Characterisation of a Reference Transcriptome for Lentil (Lens culinaris Medik.)
Next Article in Special Issue
Multiple Activities of Punica granatum Linne against Acne Vulgaris
Previous Article in Journal
Impact of SNPs on Protein Phosphorylation Status in Rice (Oryza sativa L.)
Previous Article in Special Issue
Modulatory Mechanism of Nociceptive Neuronal Activity by Dietary Constituent Resveratrol
Article Menu
Issue 11 (November) cover image

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2016, 17(11), 1888; doi:10.3390/ijms17111888

Procyanidin A2 Modulates IL-4-Induced CCL26 Production in Human Alveolar Epithelial Cells

1
Food and Wellness Group, The New Zealand Institute for Plant & Food Research Ltd., Palmerston North 4474, New Zealand
2
School of Food and Nutrition, Massey Institute of Food Science and Technology, Massey University, Palmerston North 4442, New Zealand
*
Author to whom correspondence should be addressed.
Academic Editors: Paula Andrade and Patrícia Valentão
Received: 6 October 2016 / Revised: 8 November 2016 / Accepted: 8 November 2016 / Published: 12 November 2016
(This article belongs to the Special Issue Natural Anti-Inflammatory Agents)
View Full-Text   |   Download PDF [1793 KB, uploaded 12 November 2016]   |  

Abstract

Allergic asthma is an inflammatory lung disease that is partly sustained by the chemokine eotaxin-3 (CCL26), which extends eosinophil migration into tissues long after allergen exposure. Modulation of CCL26 could represent a means to mitigate airway inflammation. Here we evaluated procyanidin A2 as a means of modulating CCL26 production and investigated interactions with the known inflammation modulator, Interferon γ (IFNγ). We used the human lung epithelial cell line A549 and optimized the conditions for inducing CCL26. Cells were exposed to a range of procyanidin A2 or IFNγ concentrations for varied lengths of time prior to an inflammatory insult of interleukin-4 (IL-4) for 24 h. An enzyme-linked immunosorbent assay was used to measure CCL26 production. Exposing cells to 5 μM procyanidin A2 (prior to IL-4) reduced CCL26 production by 35% compared with control. Greatest inhibition by procyanidin A2 was seen with a 2 h exposure prior to IL-4, whereas IFNγ inhibition was greatest at 24 h. Concomitant incubation of procyanidin A2 and IFNγ did not extend the inhibitory efficacy of procyanidin A2. These data provide evidence that procyanidin A2 can modulate IL-4-induced CCL26 production by A549 lung epithelial cells and that it does so in a manner that is different from IFNγ. View Full-Text
Keywords: airway inflammation; eotaxin-3 (CCL26); IFNγ; IL-4; procyanidin A2 airway inflammation; eotaxin-3 (CCL26); IFNγ; IL-4; procyanidin A2
Figures

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Supplementary material

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Coleman, S.L.; Kruger, M.C.; Sawyer, G.M.; Hurst, R.D. Procyanidin A2 Modulates IL-4-Induced CCL26 Production in Human Alveolar Epithelial Cells. Int. J. Mol. Sci. 2016, 17, 1888.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top