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BACKGROUND: Populations that consume procyanidin-rich diets are less susceptible to inflammatory disease. Allergic asthma is an inflammatory lung disease perpetuated by a hyperreactive airway epithelium and eosinophil infiltration into the lung. Eotaxin-1 (CCL11) mediates eosinophil migration into tissues and its modulation could represent a means to assist the management of airway inflammation. OBJECTIVE: Here we evaluated procyanidins as a means of modulating CCL11 production in vitro. METHODS: We used human lung epithelial cells (A549) and optimized the conditions to induce CCL11 production in vitro. Cells were exposed to procyanidins for 6 h prior to an inflammatory insult of 5 ng/mL IL-4 with 5 ng/mL TNF for 48 h. An enzyme-linked immunosorbent assay was used to measure CCL11 production. RESULTS: Cells exposed to 5 M procyanidin A2 prior to the inflammatory challenge showed significantly inhibited (36%) CCL11 production. Under the same conditions, procyanidins B1 and B2 elicited no effect. Furthermore, combinations of procyanidins A2 and B2 (5 M total) demonstrated no evidence of a synergistic interaction. CONCLUSIONS: These data demonstrate that the regulation of CCL11 by lung epithelial cells is not ubiquitous among the three investigated procyanidins. We demonstrate a differential inhibition of CCL11 by A-type and B-type procyanidins. This evidence supports further studies into procyanidins, specifically A-type, for managing inappropriate airway inflammation.

The in vitro evaluation of isolated procyanidins as modulators of cytokine-induced eotaxin production in human alveolar epithelial cells