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A herbal preparation Imupret® inhibits LPS and IL-1β-induced release of IL-8 and human β-defensin 2 in lung epithelial A549 cells
Airway inflammation, frequently associated with neutrophil inflammation, is a hallmark of numerous diseases. The recruitment of neutrophils in airway inflammation may account for the generation of interleukin 8 (IL-8), the prototypic CXC chemokine and neutrophils agonist. IL-8 is also generated by tissue cells after stimulation by endotoxin or by proinflammatory cytokines e.g. interleukin-1β (IL-1β). To evaluate the effectiveness of Imupret® in the modulation of airway inflammation LPS and IL-1β primed A549 bronchial epithelial cells were analyzed for the production of IL-8 and human β-defensin 2 (hBD-2). For the stimulation of A549 cells the LPS from an important respiratory pathogen Pseudomonas aeruginosa (100µg/ml) and IL-1β (50ng/ml) were used. Dexamethasone (10-7M) was used as positive anti-inflammatory control. IL-8 and hBD-2 production were detected in the supernatants of A549 cells after 18h incubation with commercially available ELISA test kits (Bender MedSystems, CA; Phoenix Pharmaceuticals, CA). Imupret® dissolved in single solvents (bidest H2O, cell culture medium, 70% (v/v) ethanol and DMSO) at non toxic concentrations in the range between 0.01 and 100µg/ml were investigated. A549 cells expressed toll-like receptor 4 (TLR4), which is required for hBD-2 induction. Production of IL-8 after stimulation by both LPS and IL-1β in A549 cells was significantly inhibited by pre-treatment with Imupret®. IL-8 level of LPS-stimulated cells was decreased about 20–40% by Imupret® (1–100µg/ml) treatment, however in Il-1β primed cells 30% (100µg/ml) and 20% (10µg/ml) decreases were detected. In non-stimulated A549 cells the basal level of IL-8 also decreased. IL-1β up-regulated level of hBD-2 was inhibited by Imupret® at a concentration range between 0.1–100µg/ml. In conclusion, Imupret® may help to suppress airway inflammation by inhibiting IL-8 production and down regulation of hBD-2 (increased level in chronic inflammatory diseases) in epithelial cells.