Abstract
Background
Histamine, a key chemical mediator in allergic reaction, exhibits an array of pro-inflammatory effects that include the activation of fibroblasts. The aim of this study was to evaluate whether histamine could stimulate nasal polyp-derived fibroblasts to express vascular cell adhesion molecule (VCAM)-1, a surface molecule involved in structural-inflammatory cell interaction and whether levocetirizine could inhibit this induction.
Methods
Primary nasal polyp tissue-derived fibroblasts were stimulated with histamine (10–1000 μM) or interleukin (IL)-4 plus tumor necrosis factor (TNF)-α (0.5–5 ng/mL) and VCAM-1 expression was evaluated by flow cytometry analysis. The inhibitory effect of the selective H1-antagonist levocetirizine (0.01–10.0μM) on VCAM-1 expression was also tested.
Results
Compared with unstimulated cultures, histamine or IL-4 + TNF-α, at the highest concentrations tested, significantly increase VCAM-1 expression (p < 0.05). To evaluate the ability of levocetirizine to downregulate VCAM-1 expression, fibroblasts were stimulated with histamine (1000 μM) or IL-4 + TNF-α (5 ng/mL), in the presence of the drug (0.01–10.0 μM). The histamine-induced VCAM-1 expression was effectively inhibited by levocetirizine (0.1–10.0 μM) (p < 0.05). No effect of the drug on IL-4 + TNF-α-induced VCAM-1 expression was observed.
Conclusions
Histamine upregulates VCAM-1 expression on nasal polyp-derived fibroblasts and this phenomenon, relevant to allergic late-phase inflammation, is effectively inhibited by levocetirizine.
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