2. Academic Validation
  3. Procyanidin A2 Modulates IL-4-Induced CCL26 Production in Human Alveolar Epithelial Cells

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

  • Int J Mol Sci. 2016 Nov 12;17(11):1888. doi: 10.3390/ijms17111888.
Sara L Coleman 1 2,  Marlena C Kruger 3,  Gregory M Sawyer 4,  Roger D Hurst 5
Affiliations

Affiliations

  • 1 Food and Wellness Group, The New Zealand Institute for Plant & Food Research Ltd., Palmerston North 4474, New Zealand. sara.coleman@plantandfood.co.nz.
  • 2 School of Food and Nutrition, Massey Institute of Food Science and Technology, Massey University, Palmerston North 4442, New Zealand. sara.coleman@plantandfood.co.nz.
  • 3 School of Food and Nutrition, Massey Institute of Food Science and Technology, Massey University, Palmerston North 4442, New Zealand. m.c.kruger@massey.ac.nz.
  • 4 Food and Wellness Group, The New Zealand Institute for Plant & Food Research Ltd., Palmerston North 4474, New Zealand. greg.sawyer@plantandfood.co.nz.
  • 5 Food and Wellness Group, The New Zealand Institute for Plant & Food Research Ltd., Palmerston North 4474, New Zealand. roger.hurst@plantandfood.co.nz.
PMID: 27845745 DOI: 10.3390/ijms17111888
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.

Keywords

IFNγ; IL-4; airway inflammation; eotaxin-3 (CCL26); procyanidin A2.

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