Purpose: Trauma-induced suppression of cellular immune function likely contributes to sepsis, multiple organ dysfunction syndrome and death. T cell proliferation decreases after traumatic stress. The addition of prostaglandin E(2) (PGE(2)), which depresses immune function after hemorrhage and trauma, to T-cells decreases T-cell proliferation; and hypertonic saline restores PGE(2)-induced T-cell suppression. Recently, it has become apparent that macrophage migration inhibitory factor (MIF) plays a central role in several immune responses, including T-cell proliferation. However, the role of MIF in mediating hypertonic saline (HTS) restoration of T cell dysfunction is unknown. Therefore, we hypothesize that T cell immune restoration by HTS occurs, at least in part, by a MIF-mediated mechanism.
Methods: Jurkat cells were cultured in Roswell Park Memorial Institute media, at a final concentration of 2.5 × 10(6) cell/mL. The effects of HTS on T-cell proliferation following PGE(2)-induced suppression were evaluated in Jurkat cells: HTS at 20 or 40 mmol/L above isotonicity was added. MIF levels were determined by enzyme-linked immunosorbent assay and western blot analysis.
Results: PGE(2) caused a 15.0% inhibition of Jurkat cell proliferation, as compared to the control. MIF levels decreased in PGE(2)-suppressed cells, as compared to the control. MIF levels were higher in cells treated with HTS than PGE(2)-stimulated cells.
Conclusion: The role of HTS in restoring Jurkat cells proliferation suppressed by PGE(2), at least in part, should be mediated through a MIF pathway.
Keywords: Hypertonic solutions; Injuries; Macrophage Migration-Inhibitory factors; Prostaglandins E; T-lymphocytes.