Akademik Veri Yönetim Sistemi
Jundishapur Journal of Microbiology, cilt.19, sa.1, 2026 (SCI-Expanded, Scopus)
Background: The SARS-CoV-2 spike protein, a key component in viral entry, has been implicated in modulating inflammatory responses even in the absence of complete viral infection. Spike protein exposure can alter signaling pathways in colon epithelial cells, leading to increased expression of proinflammatory cytokines and disruption of epithelial barrier integrity. Objectives: This study evaluates the time-dependent effects of recombinant spike protein on proinflammatory gene expression and cytokine release in lung (BEAS-2B) and colon (CRL-1831) epithelial cells. Methods: BEAS-2B and CRL-1831 cells were treated with varying doses of spike protein, and samples were collected at 12, 24, 48, and 72 hours. Cell viability was assessed via XTT assay. Quantitative PCR (qPCR) was used to measure IFN-γ, TNF-α, IL-6, and IL-1β mRNA levels. Cytokine secretion was analyzed via ELISA. Results: In BEAS-2B cells, spike protein induced a transient increase in IFN-γ at early time points, followed by a reduction in IFN-γ and IL-6 at later times. Conversely, CRL-1831 cells demonstrated sustained or delayed increases in TNF-α and IFN-γ expression, with notable IL-6 fluctuation. ELISA data confirmed these trends in cytokine secretion profiles. No significant cytotoxicity was observed across the tested conditions. Conclusions: The spike protein elicits distinct temporal inflammatory responses in lung and colon epithelial cells, underscoring tissue-specific susceptibility and regulatory mechanisms in SARS-CoV-2 pathogenesis. While some previous studies have examined individual components of SARS-CoV-2, the present study's specific focus on the time-dependent, differential effects of the spike protein on two distinct epithelial cell types (lung and colon) appears to be a unique contribution to the field. These findings may contribute to understanding gastrointestinal and respiratory complications observed in COVID-19 patients.