Substance P potentiates TGF-β1 production in lung epithelial cell lines
Transforming growth factor-beta (TGF-beta) is one of the most important cytokines implicated in growth, differentiation, repair and also the pathogenesis of the lung fibrosis by its stimulatory effect on extracellular matrix deposition. Pulmonary epithelial cells are considered as a source of TGF-beta in lung. Substance P (SP), as a neuroimmunomodulator has elevated levels in inflamed airways and although it has significant role in the pathogenesis of the lung fibrosis, but its effect on transforming growth factor -beta (TGF-beta) production of the lung epithelial cells (and so its regulatory potential) remains unclear. In this study TGFbeta-1 levels in supernatants of the normal (BEAS-2B) and cancerous (A549) lung epithelial cell line cultures at the presence of various concentrations of SP were examined and MTT assay was performed to evaluate cells viability. We have observed that SP (without any other stimulator) significantly augments TGF-beta production of both BEAS and A54 cells and this effect is inhibited by NK1-receptor antagonist (CP-96345). We have also observed that the viability of cells did not significantly affect at the presence of SP. It can be concluded that SP can directly modulate the release of TGF-beta from human bronchial epithelial cell line and thereby participates in various lung functions or pathologic conditions.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.