TNF-α upregulates VCAM-1 and NF-κB in fibroblasts from nasal polyps

Objective Lung and synovial fibroblasts produce VCAM-1 in response to TNF-α. However, the massive infiltration of eosinophils, the effects of the increased amount of TNF-α and the production of VCAM-1 in human nasal polyp fibroblasts are not yet fully understood. The present study examines the role of VCAM-1 and the molecular mechanism of its expression in nasal fibroblasts. Methods Nasal fibroblasts were isolated from human nasal polyps and after four passages, the cells were stimulated with TNF-α and VCAM-1 expression was examined by ELISA, flow cytometry, and RT-PCR. The activation of NF-κB induced by TNF-α was determined by electrophoretic mobility shift assays and the influence on the expression of VCAM-1 was investigated. Results VCAM-1 protein and mRNA were expressed in unstimulated controls and remarkably increased by TNF-α stimulation. NF-κB activity was enhanced by TNF-α stimulation and remarkably suppressed by NF-κB proteasome inhibitor. Conclusions The present study discovered that nasal fibroblasts produce VCAM-1 protein and mRNA and that production is increased by TNF-α stimulation. Furthermore, VCAM-1 expression in nasal fibroblasts is induced through an NF-κB-dependent pathway. These findings might provide a rationale for using NF-κB inhibitors as a treatment for nasal inflammatory diseases such as polyps.