Effect of hypertonic saline and macrophage migration inhibitory factor in restoration of T cell dysfunction.
10.4174/jkss.2011.81.4.229
- Author:
Young Hoon YOON
1
;
Sung Hyuk CHOI
;
Yun Sik HONG
;
Sung Woo LEE
;
Sung Woo MOON
;
Han Jin CHO
;
Cheul HAN
;
Young Jin CHEON
;
Vishal BANSAL
Author Information
1. Department of Emergency Medicine, Korea University College of Medicine, Seoul, Korea. kuedchoi@korea.ac.kr
- Publication Type:Original Article
- Keywords:
Hypertonic solutions;
Macrophage Migration-Inhibitory factors;
Prostaglandins E;
Injuries;
T-lymphocytes
- MeSH:
Blotting, Western;
Cell Proliferation;
Dinoprostone;
Enzyme-Linked Immunosorbent Assay;
Hemorrhage;
Humans;
Hypertonic Solutions;
Jurkat Cells;
Macrophage Migration-Inhibitory Factors;
Macrophages;
Multiple Organ Failure;
Negotiating;
Prostaglandins E;
Sepsis;
T-Lymphocytes
- From:Journal of the Korean Surgical Society
2011;81(4):229-234
- CountryRepublic of Korea
- Language:English
-
Abstract:
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 E2 (PGE2), which depresses immune function after hemorrhage and trauma, to T-cells decreases T-cell proliferation; and hypertonic saline restores PGE2-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 x 106 cell/mL. The effects of HTS on T-cell proliferation following PGE2-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: PGE2 caused a 15.0% inhibition of Jurkat cell proliferation, as compared to the control. MIF levels decreased in PGE2-suppressed cells, as compared to the control. MIF levels were higher in cells treated with HTS than PGE2-stimulated cells. CONCLUSION: The role of HTS in restoring Jurkat cells proliferation suppressed by PGE2, at least in part, should be mediated through a MIF pathway.
