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Published on: January 7, 2019
Hypertonic saline downregulate the production level of lipopolysaccharide-induced migration inhibitory factor in
Cheul Han1, Sung-Hyuk Choi, Young-Hoon Yoon
1Department of Emergency Medicine, Ewha Womans University Hospital, Seoul, Korea.
Purpose:
Macrophage migration inhibitory factor (MIF) may serve as a general marker for systemic inflammation in septic and nonseptic acute critical illness. Additionally, our previous experiment has demonstrated that immunosuppressant Prostaglandin E(2) (PGE(2)) lowered MIF levels and inhibited T-cells proliferation when compared to control levels. The addition of hypertonic saline (HTS) increased MIF production as compared with PGE(2)-stimulated T-cells in concordance with restore PGE(2)-suppressed T-cells proliferation. Generally, HTS has been well known for its anti-inflammatory effect so far. Therefore, the experiments were conducted to evaluate MIF after stimulating lipopolysaccharide (LPS) either in the presence or absence of HTS in monocyte, in response to early phase injury.
Methods:
Human acute monocytic leukemic cell line (THP-1) cells were cultured in RPMI media, to a final concentration of 1 × 10(6) cells/mL. The effect of HTS on LPS-induced MIF was evaluated in monocyte with 1 µg/mL LPS. HTS at 10, 20 or 40 mmol/L above isotonicity was added. MIF concentrations of the supernatant were determined by enzyme-linked immunosorbent assay, and cell lysates were used for Western blots analysis to determine the MIF expression.
Results:
MIF concentrations in the cell supernatant increased in LPS-induced cells compared to control cells. Also, levels of MIF protein expression were higher in LPS stimulating cells. However, the addition of HTS to LPS stimulated cell restored MIF concentrations and MIF expression.
Conclusion:
The role of HTS in maintaining physiological balance in human beings, at least in part, should be mediated through the MIF pathway.
Insights
Hypertonic saline (HTS) counteracts lipopolysaccharide (LPS)-induced increases in macrophage migration inhibitory factor (MIF) in monocytes. This suggests HTS may play a role in regulating inflammation through the MIF pathway.
Area of Science:
- Immunology
- Cell Biology
- Critical Care Medicine
Background:
- Macrophage migration inhibitory factor (MIF) is a marker of systemic inflammation in critical illness.
- Prostaglandin E(2) (PGE(2)), an immunosuppressant, reduces MIF levels and T-cell proliferation.
- Hypertonic saline (HTS) is known for its anti-inflammatory effects, but its impact on MIF requires further investigation.
Purpose of the Study:
- To investigate the effect of HTS on lipopolysaccharide (LPS)-induced MIF production in monocytes.
- To evaluate the role of MIF as a mediator of HTS's anti-inflammatory effects during early-phase injury.
Main Methods:
- Human acute monocytic leukemia (THP-1) cells were stimulated with LPS.
- HTS was added at varying concentrations (10, 20, 40 mmol/L above isotonicity).
- MIF concentrations were measured using ELISA, and protein expression was analyzed via Western blot.
Main Results:
- LPS stimulation increased MIF concentrations and protein expression in monocytes.
- The addition of HTS to LPS-stimulated cells reversed these increases, restoring normal MIF levels.
- HTS demonstrated a regulatory effect on LPS-induced MIF production.
Conclusions:
- HTS may modulate systemic inflammation, at least partly, by regulating the MIF pathway.
- The findings suggest a potential therapeutic role for HTS in inflammatory conditions.
- MIF is implicated in the physiological balance maintained by HTS.
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