A biphasic effect of tumor necrosis factor-α on RPMI 2650 cell line in vitro

Tumor necrosis factor-α (TNFα) is a key proinflammatory cytokine; its level increased in inflammatory diseases of the upper respiratory tract. In this study, the dose- and time-dependent effects of TNFα (1-100 ng/ml, 6-48 h) on the RPMI 2650 cell line, a model of nasal epithelium, have been investigated. Short-term exposure (6 h) caused activation of NF-κB and an increase in the levels of the intercellular contact proteins E-cadherin and ZO-1, without a significant effect on cell viability. Long-term exposure (24-48 h) led to an increase in the level of pro-IL-1β, activation of apoptosis, and a decrease in cell viability. At the same time, a decrease in the level of intercellular contact proteins was noted. Thus, short-term exposure to TNFα can exert a protective effect by increasing the density of intercellular contacts, while during prolonged exposure it triggers apoptosis and reduces the density of intercellular contacts, which can contribute to increased permeability of the cell layer.