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Published on: June 25, 2015
Transcriptomic profiling of TSST-1-induced cytotoxicity and inflammatory responses in human vaginal epithelial cells
Xueling Luo1,2, Yue Yuan2,3, Ke Chen1,2
1Department of Infectious Diseases, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Objective:
Toxic shock syndrome toxin-1 (TSST-1) is a critical superantigen produced by certain staphylococcal strains, closely associated with menstrual toxic shock syndrome and mucosal inflammation. While the systemic superantigenic function of TSST-1 is well-established, its early cytotoxic and inflammatory effects on human vaginal epithelial cells (HVEC) remain poorly characterized. This study, therefore, sought to investigate the initial temporal dynamics of TSST-1-induced changes in cell viability, inflammatory cytokine responses, epithelial stress-related responses, and barrier-associated transcriptional changes in a human vaginal epithelial cell model, along with transcriptomic analysis.
Methods:
We evaluated the impact of recombinant TSST-1 on HVEC at different doses and treatment durations. Subsequent exposure assessments included cell viability, apoptosis, and cell cycle distribution via flow cytometry, alongside inflammatory gene expression and transcriptomic profiling.
Results:
TSST-1 reduced cell viability and proliferation in a dose-and time-dependent manner due to increased apoptosis and G1-phase accumulation. Notably, early exposure did not result in a uniform upregulation of all inflammatory mediators; rather, multiple cytokines exhibited dose-dependent segmented response patterns instead of a linear increase. RNA sequencing analysis of samples treated with 125 or 1000 ng/mL TSST-1 for 48 h revealed dose-associated transcriptional changes involving chemokine signaling, cytokine-receptor interactions, epithelial stress-related pathways, and glycolysis-related pathways. Notably the moderate-dose group showed a higher number of statistically defined differentially expressed genes than the high-dose group, suggesting a non-linear dose-associated transcriptional pattern.
Conclusion:
These findings demonstrate that TSST-1 can trigger cytotoxicity, apoptosis, cell cycle disruption, and a graded inflammatory response in vaginal epithelial cells, providing a systematic transcriptomic framework for understanding the early mucosal responses induced by TSST-1.
