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논문 기본 정보

자료유형
학술저널
저자정보
Young-Hoon Yoon (Korea University) Sung-Hyuk Choi (Korea University) Yun-Sik Hong (Korea University) Sung-Woo Lee (Korea University) Sung-Woo Moon (Korea University) Han-Jin Cho (Korea University) Cheul Han (Ewha Womans University) Young-Jin Cheon (Ewha Womans University) Vishal Bansal (University of California San Diego)
저널정보
대한외과학회 Annals of Surgical Treatment and Research 대한외과학회지 Vol.81 No.4
발행연도
2011.10
수록면
229 - 234 (6page)

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초록· 키워드

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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 × 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.

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Purpose
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