HEp-2 cells exposed to glucocorticoids and LPS undergo organelle damage and apoptosis.

Glucocorticoids are potent anti-inflammatory and immunosuppressive agents that are known to affect T cell-mediated inflammation by the inhibition of cellular proliferation and cytokine production. The literature is lacking in explaining the mode of action of such agents on the epithelial cells. Therefore epithelial cells (HEp-2) were used to determine the effects of cortisol administration or cortisol in the presence of LPS on the cells metabolic functions. Cells were treated with physiological concentrations of cortisol or cortisol + LPS for periods of 24, 48 and 72 hours. After each phase cell number, cellular damage and cellular morphology were determined. The results indicated that cortisol and cortisol + LPS treated cells inhibited cellular proliferation as well as cellular MDA levels as early as 24 hours. Analysis of programmed cell death by apoptosis staining for Annexin V revealed that cortisol and cortisol + LPS treated cells had lower positive response. However, these differences do not take into consideration the reduction in cell number in the cortisol and cortisol + LPS treated cells. Overall, the results indicate that cortisol has a remarkable effect on HEp-2 cellular proliferation similar to the reduction seen in the literature for T-cells. In addition to reduction in cellular number the cell's ability to adjust to a bacterial challenge may be directly altered. This information is important for managing patients who are immuno-suppressed with s respiratory tract infections.