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.
Highlights
Procyanidins are polyphenolic secondary plant metabolites that are recognized as biologically active in the context of human health
These experiments demonstrated that 5 ng/mL IL-4 for 24 h allowed for a robust induction of CCL26 production in A549 cells
When we investigated possible coordinated interactions between procyanidin A2 and Interferon γ (IFNγ), we found no evidence of cooperative inhibition
Summary
Procyanidins are polyphenolic secondary plant metabolites that are recognized as biologically active in the context of human health. They are the product of polymerization of monomeric flavan-3-ol units by a currently undefined mechanism in plants [1]. Concentrated extracts or isolated bioactive plant compounds could supplement the typical western diet for improved health and wellbeing Inflammatory diseases, such as allergic asthma, are less prevalent in populations that consume procyanidin-rich diets [6,7]. TThhee ttiimmee ccoouurrssee ffoorr CCCCLL2266 pprroodduuccttiioonn ffoolllloowwiinngg 55nngg//mmLL IILL--44 rraannggiinngg ffrroomm 11 ttoo 7722 hh iiss sshhoowwnn iinn FFiigguurree 22BB. These data correspond to a 16% inhibition of CCL26 production by DMSO. Time-Dependent Inhibition of CCL26 (Eotaxin-3) by Procyanidin A2 and IFNγ (Interferon γ). Different letters “a” and “b” represent statistical difference, p < 0.05
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