Effect of hypertonic saline and macrophage migration inhibitory factor in restoration of T cell dysfunction
- Authors
- Yoon, Young-Hoon; Choi, Sung-Hyuk; Hong, Yun-Sik; Lee, Sung-Woo; Moon, Sung-Woo; Cho, Han-Jin; Han, Cheul; Cheon, Young-Jin; Bansal, Vishal
- Issue Date
- 10월-2011
- Publisher
- KOREAN SURGICAL SOCIETY
- Keywords
- Hypertonic solutions; Macrophage Migration-Inhibitory factors; Prostaglandins E; Injuries; T-lymphocytes
- Citation
- JOURNAL OF THE KOREAN SURGICAL SOCIETY, v.81, no.4, pp.229 - 234
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- JOURNAL OF THE KOREAN SURGICAL SOCIETY
- Volume
- 81
- Number
- 4
- Start Page
- 229
- End Page
- 234
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/111403
- DOI
- 10.4174/jkss.2011.81.4.229
- ISSN
- 2233-7903
- 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 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 x 10(6) cell/mL. The effects of HTS on T-cell proliferation following PGE(2)-induced suppression were evaluated in Jurkat 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 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.
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Collections - College of Medicine > Department of Medical Science > 1. Journal Articles
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