Arginine is Essential in Reversing Prostaglandin E2 T-Cell Suppression by Hypertonic Saline

Sung Hyuk Choi, Vishal Bansal, Todd Costantini, Jim Putnam, William Loomis, Raul Coimbra

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Background: T-cell dysfunction after trauma is characterized by decreased T-cell proliferation. Hypertonic saline (HS) restores T-cell proliferation by an unknown mechanism. Arginine and regulation of arginine metabolism plays an important role in normal T-cell function. We hypothesize that HS restoration of T-cell dysfunction is dependent on an arginine mediated mechanism. Material and Methods: Jurkat cells were cultured in both 0 mM and 1.14mM arginine media. Cell proliferation was suppressed using prostaglandin E2 (PGE2) and treated with HS at 20 and 40mM above isotonicity. Arginase activity was blocked by norNOHA. Cell proliferation, arginase activity, and nitrite accumulation were measured. Results: PGE2 caused a 15.0% inhibition of Jurkat cell proliferation compared with control (P < 0.05). HS reversed PGE2 suppressed Jurkat cell proliferation to normal. PGE2 suppression decreased mean arginase activity (66.5 ± 15 nmol/min/mg) compared with controls (98.4 ± 14 nmol/min/mg) (P < 0.05). Cells treated with HS had higher arginase activity (123.8 ± 38 nmol/min/mg) then PGE2 suppressed cells and controls (P <.05). Conversely, nitrite was decreased by 14.5% ± 3.1% in HS treated cells compared with PGE2 suppression (P < 0.05). HS did not restore PGE2 cell suppression when arginase I was blocked by norNOHA, nor when cells were cultured in arginine-free media. Conclusions: Arginine is essential in restoring Jurkat cell proliferation by HS. HS may restore T-cell dysfunction by increasing arginine transport and arginine metabolism by arginase I. HS treatment will not restore suppressed T-cell proliferation without adequate extracellular concentrations of arginine.

Original languageEnglish
Pages (from-to)83-89
Number of pages7
JournalJournal of Surgical Research
Volume156
Issue number1
DOIs
Publication statusPublished - 2009 Sep 1

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Dinoprostone
Arginine
Arginase
T-Lymphocytes
Cell Proliferation
Jurkat Cells
Nitrites
Cultured Cells
Wounds and Injuries

Keywords

  • arginase
  • arginine
  • hypertonic saline
  • immune suppression
  • T-cells
  • trauma

ASJC Scopus subject areas

  • Surgery

Cite this

Arginine is Essential in Reversing Prostaglandin E2 T-Cell Suppression by Hypertonic Saline. / Choi, Sung Hyuk; Bansal, Vishal; Costantini, Todd; Putnam, Jim; Loomis, William; Coimbra, Raul.

In: Journal of Surgical Research, Vol. 156, No. 1, 01.09.2009, p. 83-89.

Research output: Contribution to journalArticle

Choi, Sung Hyuk ; Bansal, Vishal ; Costantini, Todd ; Putnam, Jim ; Loomis, William ; Coimbra, Raul. / Arginine is Essential in Reversing Prostaglandin E2 T-Cell Suppression by Hypertonic Saline. In: Journal of Surgical Research. 2009 ; Vol. 156, No. 1. pp. 83-89.
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abstract = "Background: T-cell dysfunction after trauma is characterized by decreased T-cell proliferation. Hypertonic saline (HS) restores T-cell proliferation by an unknown mechanism. Arginine and regulation of arginine metabolism plays an important role in normal T-cell function. We hypothesize that HS restoration of T-cell dysfunction is dependent on an arginine mediated mechanism. Material and Methods: Jurkat cells were cultured in both 0 mM and 1.14mM arginine media. Cell proliferation was suppressed using prostaglandin E2 (PGE2) and treated with HS at 20 and 40mM above isotonicity. Arginase activity was blocked by norNOHA. Cell proliferation, arginase activity, and nitrite accumulation were measured. Results: PGE2 caused a 15.0{\%} inhibition of Jurkat cell proliferation compared with control (P < 0.05). HS reversed PGE2 suppressed Jurkat cell proliferation to normal. PGE2 suppression decreased mean arginase activity (66.5 ± 15 nmol/min/mg) compared with controls (98.4 ± 14 nmol/min/mg) (P < 0.05). Cells treated with HS had higher arginase activity (123.8 ± 38 nmol/min/mg) then PGE2 suppressed cells and controls (P <.05). Conversely, nitrite was decreased by 14.5{\%} ± 3.1{\%} in HS treated cells compared with PGE2 suppression (P < 0.05). HS did not restore PGE2 cell suppression when arginase I was blocked by norNOHA, nor when cells were cultured in arginine-free media. Conclusions: Arginine is essential in restoring Jurkat cell proliferation by HS. HS may restore T-cell dysfunction by increasing arginine transport and arginine metabolism by arginase I. HS treatment will not restore suppressed T-cell proliferation without adequate extracellular concentrations of arginine.",
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AU - Choi, Sung Hyuk

AU - Bansal, Vishal

AU - Costantini, Todd

AU - Putnam, Jim

AU - Loomis, William

AU - Coimbra, Raul

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N2 - Background: T-cell dysfunction after trauma is characterized by decreased T-cell proliferation. Hypertonic saline (HS) restores T-cell proliferation by an unknown mechanism. Arginine and regulation of arginine metabolism plays an important role in normal T-cell function. We hypothesize that HS restoration of T-cell dysfunction is dependent on an arginine mediated mechanism. Material and Methods: Jurkat cells were cultured in both 0 mM and 1.14mM arginine media. Cell proliferation was suppressed using prostaglandin E2 (PGE2) and treated with HS at 20 and 40mM above isotonicity. Arginase activity was blocked by norNOHA. Cell proliferation, arginase activity, and nitrite accumulation were measured. Results: PGE2 caused a 15.0% inhibition of Jurkat cell proliferation compared with control (P < 0.05). HS reversed PGE2 suppressed Jurkat cell proliferation to normal. PGE2 suppression decreased mean arginase activity (66.5 ± 15 nmol/min/mg) compared with controls (98.4 ± 14 nmol/min/mg) (P < 0.05). Cells treated with HS had higher arginase activity (123.8 ± 38 nmol/min/mg) then PGE2 suppressed cells and controls (P <.05). Conversely, nitrite was decreased by 14.5% ± 3.1% in HS treated cells compared with PGE2 suppression (P < 0.05). HS did not restore PGE2 cell suppression when arginase I was blocked by norNOHA, nor when cells were cultured in arginine-free media. Conclusions: Arginine is essential in restoring Jurkat cell proliferation by HS. HS may restore T-cell dysfunction by increasing arginine transport and arginine metabolism by arginase I. HS treatment will not restore suppressed T-cell proliferation without adequate extracellular concentrations of arginine.

AB - Background: T-cell dysfunction after trauma is characterized by decreased T-cell proliferation. Hypertonic saline (HS) restores T-cell proliferation by an unknown mechanism. Arginine and regulation of arginine metabolism plays an important role in normal T-cell function. We hypothesize that HS restoration of T-cell dysfunction is dependent on an arginine mediated mechanism. Material and Methods: Jurkat cells were cultured in both 0 mM and 1.14mM arginine media. Cell proliferation was suppressed using prostaglandin E2 (PGE2) and treated with HS at 20 and 40mM above isotonicity. Arginase activity was blocked by norNOHA. Cell proliferation, arginase activity, and nitrite accumulation were measured. Results: PGE2 caused a 15.0% inhibition of Jurkat cell proliferation compared with control (P < 0.05). HS reversed PGE2 suppressed Jurkat cell proliferation to normal. PGE2 suppression decreased mean arginase activity (66.5 ± 15 nmol/min/mg) compared with controls (98.4 ± 14 nmol/min/mg) (P < 0.05). Cells treated with HS had higher arginase activity (123.8 ± 38 nmol/min/mg) then PGE2 suppressed cells and controls (P <.05). Conversely, nitrite was decreased by 14.5% ± 3.1% in HS treated cells compared with PGE2 suppression (P < 0.05). HS did not restore PGE2 cell suppression when arginase I was blocked by norNOHA, nor when cells were cultured in arginine-free media. Conclusions: Arginine is essential in restoring Jurkat cell proliferation by HS. HS may restore T-cell dysfunction by increasing arginine transport and arginine metabolism by arginase I. HS treatment will not restore suppressed T-cell proliferation without adequate extracellular concentrations of arginine.

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