Immunoregulation of transfusion-induced immunosuppression with inhibitors of the arachidonic acid metabolism

Richard V Perez, G. F. Babcock, J. W. Alexander

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

To further define the role of arachidonic acid (AA) metabolites in transfusion-induced immunosuppression (TII), the effects of pharmacological manipulation of AA metabolism were examined in a rodent model. If the prostaglandins of the E series are mediators of TII, as has been recently hypothesized, then inhibition of cyclooxygenase (indomethacin) should abrogate whereas inhibition of lipoxygenase (nordihydroguaiaretic acid [NDGA]), or thromboxane synthetase (4-63557A) could potentiate the transfusion effect. Lewis rats received donor-specific transfusions from Buffalo rats in conjunction with one of the above inhibitors. Two weeks later they received intraabdominal Buffalo heart allografts or were used for one-way mixed lymphocyte reactions. Cyclooxygenase inhibition partially abrogated TII with shortened cardiac allograft survival. Lipoxygenase inhibition augmented TII, with depression of MLR and prolongation of allograft survival. Thromboxane synthetase inhibition had no effect. These results indicate that AA metabolites play a role in TII, and that immunoregulation via pharmacological manipulation of AA metabolism is possible.

Original languageEnglish (US)
Pages (from-to)85-87
Number of pages3
JournalTransplantation
Volume48
Issue number1
StatePublished - 1989
Externally publishedYes

Fingerprint

Arachidonic Acid
Immunosuppression
Thromboxane-A Synthase
Allografts
Lipoxygenase
Buffaloes
Prostaglandin-Endoperoxide Synthases
Pharmacology
Masoprocol
Mixed Lymphocyte Culture Test
Prostaglandins E
Indomethacin
Rodentia

ASJC Scopus subject areas

  • Immunology
  • Transplantation

Cite this

Immunoregulation of transfusion-induced immunosuppression with inhibitors of the arachidonic acid metabolism. / Perez, Richard V; Babcock, G. F.; Alexander, J. W.

In: Transplantation, Vol. 48, No. 1, 1989, p. 85-87.

Research output: Contribution to journalArticle

@article{fa76e849967140aebc230a67f8533a8c,
title = "Immunoregulation of transfusion-induced immunosuppression with inhibitors of the arachidonic acid metabolism",
abstract = "To further define the role of arachidonic acid (AA) metabolites in transfusion-induced immunosuppression (TII), the effects of pharmacological manipulation of AA metabolism were examined in a rodent model. If the prostaglandins of the E series are mediators of TII, as has been recently hypothesized, then inhibition of cyclooxygenase (indomethacin) should abrogate whereas inhibition of lipoxygenase (nordihydroguaiaretic acid [NDGA]), or thromboxane synthetase (4-63557A) could potentiate the transfusion effect. Lewis rats received donor-specific transfusions from Buffalo rats in conjunction with one of the above inhibitors. Two weeks later they received intraabdominal Buffalo heart allografts or were used for one-way mixed lymphocyte reactions. Cyclooxygenase inhibition partially abrogated TII with shortened cardiac allograft survival. Lipoxygenase inhibition augmented TII, with depression of MLR and prolongation of allograft survival. Thromboxane synthetase inhibition had no effect. These results indicate that AA metabolites play a role in TII, and that immunoregulation via pharmacological manipulation of AA metabolism is possible.",
author = "Perez, {Richard V} and Babcock, {G. F.} and Alexander, {J. W.}",
year = "1989",
language = "English (US)",
volume = "48",
pages = "85--87",
journal = "Transplantation",
issn = "0041-1337",
publisher = "Lippincott Williams and Wilkins",
number = "1",

}

TY - JOUR

T1 - Immunoregulation of transfusion-induced immunosuppression with inhibitors of the arachidonic acid metabolism

AU - Perez, Richard V

AU - Babcock, G. F.

AU - Alexander, J. W.

PY - 1989

Y1 - 1989

N2 - To further define the role of arachidonic acid (AA) metabolites in transfusion-induced immunosuppression (TII), the effects of pharmacological manipulation of AA metabolism were examined in a rodent model. If the prostaglandins of the E series are mediators of TII, as has been recently hypothesized, then inhibition of cyclooxygenase (indomethacin) should abrogate whereas inhibition of lipoxygenase (nordihydroguaiaretic acid [NDGA]), or thromboxane synthetase (4-63557A) could potentiate the transfusion effect. Lewis rats received donor-specific transfusions from Buffalo rats in conjunction with one of the above inhibitors. Two weeks later they received intraabdominal Buffalo heart allografts or were used for one-way mixed lymphocyte reactions. Cyclooxygenase inhibition partially abrogated TII with shortened cardiac allograft survival. Lipoxygenase inhibition augmented TII, with depression of MLR and prolongation of allograft survival. Thromboxane synthetase inhibition had no effect. These results indicate that AA metabolites play a role in TII, and that immunoregulation via pharmacological manipulation of AA metabolism is possible.

AB - To further define the role of arachidonic acid (AA) metabolites in transfusion-induced immunosuppression (TII), the effects of pharmacological manipulation of AA metabolism were examined in a rodent model. If the prostaglandins of the E series are mediators of TII, as has been recently hypothesized, then inhibition of cyclooxygenase (indomethacin) should abrogate whereas inhibition of lipoxygenase (nordihydroguaiaretic acid [NDGA]), or thromboxane synthetase (4-63557A) could potentiate the transfusion effect. Lewis rats received donor-specific transfusions from Buffalo rats in conjunction with one of the above inhibitors. Two weeks later they received intraabdominal Buffalo heart allografts or were used for one-way mixed lymphocyte reactions. Cyclooxygenase inhibition partially abrogated TII with shortened cardiac allograft survival. Lipoxygenase inhibition augmented TII, with depression of MLR and prolongation of allograft survival. Thromboxane synthetase inhibition had no effect. These results indicate that AA metabolites play a role in TII, and that immunoregulation via pharmacological manipulation of AA metabolism is possible.

UR - http://www.scopus.com/inward/record.url?scp=0024342923&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024342923&partnerID=8YFLogxK

M3 - Article

C2 - 2501921

AN - SCOPUS:0024342923

VL - 48

SP - 85

EP - 87

JO - Transplantation

JF - Transplantation

SN - 0041-1337

IS - 1

ER -