Effect of β2-adrenergic receptor agonists on intercellular adhesion molecule (ICAM)-1, B7, and CD40 expression in mixed lymphocyte reaction

Ryuji Tamura, Hideo K. Takahashi, Hiromi Iwagaki, Takahito Yagi, Shuji Mori, Tadashi Yoshino, Masahiro Nishibori, Noriaki Tanaka

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Background. The plasma interleukin (IL)-18 level is elevated in acute rejection after organ transplantation. Although β2-adrenergic receptor (AR) agonists suppress the rejection of organ and tissue transplants, little is known about their action mechanisms. We examined the effects of endogenous catecholamines and β2-AR agonists on the expression of intercellular adhesion molecule (ICAM)-1, B7.1, B7.2, CD40, and CD40 ligand (CD40L) in human mixed lymphocyte reaction (MLR) and in an in vitro model of acute rejection in the presence or absence of IL-18. Methods. ICAM-1, B7.1 B7.2, CD40, and CD40L expression on monocytes was measured by flow cytometry, and the production of interferon (IFN)-γ and IL-12 was determined by enzyme-linked immunosorbent assay. Lymphocytes proliferation in MLR was measured by [ 3H]-thymidine uptake. The relevant AR subtypes were characterized using subtype-selective agonists and antagonists. Results. β2-AR agonists inhibited the expression of ICAM-1 and CD40 during MLR in the absence of IL-18. Among IL-18-induced expression of ICAM-1, B7.1, B7.2, CD40, and CD40L, β2-AR agonists inhibited ICAM-1 and CD40 expression. β2-AR agonists prevented the production of IFN-γ and IL-12 in the presence of IL-18 but had no effect in the absence of IL-18. β2-AR agonists inhibited lymphocyte proliferation in IL-18-treated MLR. Conclusions. We found that β2-AR agonists strongly inhibited the expression of ICAM-1 and CD40, irrespective of the presence or absence of IL-18, which is different from that of histamine and prostaglandin E2.

Original languageEnglish
Pages (from-to)293-301
Number of pages9
JournalTransplantation
Volume77
Issue number2
DOIs
Publication statusPublished - Jan 27 2004

Fingerprint

Adrenergic Agonists
Mixed Lymphocyte Culture Test
Interleukin-18
Intercellular Adhesion Molecule-1
CD40 Ligand
Interleukin-12
Interferons
Lymphocytes
Transplants
Organ Transplantation
Dinoprostone
Thymidine
Adrenergic Receptors
Histamine
Catecholamines
Monocytes
Flow Cytometry
Enzyme-Linked Immunosorbent Assay

ASJC Scopus subject areas

  • Transplantation
  • Immunology

Cite this

Effect of β2-adrenergic receptor agonists on intercellular adhesion molecule (ICAM)-1, B7, and CD40 expression in mixed lymphocyte reaction. / Tamura, Ryuji; Takahashi, Hideo K.; Iwagaki, Hiromi; Yagi, Takahito; Mori, Shuji; Yoshino, Tadashi; Nishibori, Masahiro; Tanaka, Noriaki.

In: Transplantation, Vol. 77, No. 2, 27.01.2004, p. 293-301.

Research output: Contribution to journalArticle

@article{b380e8c4fc2c45cea51712ad54f1bcf8,
title = "Effect of β2-adrenergic receptor agonists on intercellular adhesion molecule (ICAM)-1, B7, and CD40 expression in mixed lymphocyte reaction",
abstract = "Background. The plasma interleukin (IL)-18 level is elevated in acute rejection after organ transplantation. Although β2-adrenergic receptor (AR) agonists suppress the rejection of organ and tissue transplants, little is known about their action mechanisms. We examined the effects of endogenous catecholamines and β2-AR agonists on the expression of intercellular adhesion molecule (ICAM)-1, B7.1, B7.2, CD40, and CD40 ligand (CD40L) in human mixed lymphocyte reaction (MLR) and in an in vitro model of acute rejection in the presence or absence of IL-18. Methods. ICAM-1, B7.1 B7.2, CD40, and CD40L expression on monocytes was measured by flow cytometry, and the production of interferon (IFN)-γ and IL-12 was determined by enzyme-linked immunosorbent assay. Lymphocytes proliferation in MLR was measured by [ 3H]-thymidine uptake. The relevant AR subtypes were characterized using subtype-selective agonists and antagonists. Results. β2-AR agonists inhibited the expression of ICAM-1 and CD40 during MLR in the absence of IL-18. Among IL-18-induced expression of ICAM-1, B7.1, B7.2, CD40, and CD40L, β2-AR agonists inhibited ICAM-1 and CD40 expression. β2-AR agonists prevented the production of IFN-γ and IL-12 in the presence of IL-18 but had no effect in the absence of IL-18. β2-AR agonists inhibited lymphocyte proliferation in IL-18-treated MLR. Conclusions. We found that β2-AR agonists strongly inhibited the expression of ICAM-1 and CD40, irrespective of the presence or absence of IL-18, which is different from that of histamine and prostaglandin E2.",
author = "Ryuji Tamura and Takahashi, {Hideo K.} and Hiromi Iwagaki and Takahito Yagi and Shuji Mori and Tadashi Yoshino and Masahiro Nishibori and Noriaki Tanaka",
year = "2004",
month = "1",
day = "27",
doi = "10.1097/01.TP.0000101517.48541.7B",
language = "English",
volume = "77",
pages = "293--301",
journal = "Transplantation",
issn = "0041-1337",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

TY - JOUR

T1 - Effect of β2-adrenergic receptor agonists on intercellular adhesion molecule (ICAM)-1, B7, and CD40 expression in mixed lymphocyte reaction

AU - Tamura, Ryuji

AU - Takahashi, Hideo K.

AU - Iwagaki, Hiromi

AU - Yagi, Takahito

AU - Mori, Shuji

AU - Yoshino, Tadashi

AU - Nishibori, Masahiro

AU - Tanaka, Noriaki

PY - 2004/1/27

Y1 - 2004/1/27

N2 - Background. The plasma interleukin (IL)-18 level is elevated in acute rejection after organ transplantation. Although β2-adrenergic receptor (AR) agonists suppress the rejection of organ and tissue transplants, little is known about their action mechanisms. We examined the effects of endogenous catecholamines and β2-AR agonists on the expression of intercellular adhesion molecule (ICAM)-1, B7.1, B7.2, CD40, and CD40 ligand (CD40L) in human mixed lymphocyte reaction (MLR) and in an in vitro model of acute rejection in the presence or absence of IL-18. Methods. ICAM-1, B7.1 B7.2, CD40, and CD40L expression on monocytes was measured by flow cytometry, and the production of interferon (IFN)-γ and IL-12 was determined by enzyme-linked immunosorbent assay. Lymphocytes proliferation in MLR was measured by [ 3H]-thymidine uptake. The relevant AR subtypes were characterized using subtype-selective agonists and antagonists. Results. β2-AR agonists inhibited the expression of ICAM-1 and CD40 during MLR in the absence of IL-18. Among IL-18-induced expression of ICAM-1, B7.1, B7.2, CD40, and CD40L, β2-AR agonists inhibited ICAM-1 and CD40 expression. β2-AR agonists prevented the production of IFN-γ and IL-12 in the presence of IL-18 but had no effect in the absence of IL-18. β2-AR agonists inhibited lymphocyte proliferation in IL-18-treated MLR. Conclusions. We found that β2-AR agonists strongly inhibited the expression of ICAM-1 and CD40, irrespective of the presence or absence of IL-18, which is different from that of histamine and prostaglandin E2.

AB - Background. The plasma interleukin (IL)-18 level is elevated in acute rejection after organ transplantation. Although β2-adrenergic receptor (AR) agonists suppress the rejection of organ and tissue transplants, little is known about their action mechanisms. We examined the effects of endogenous catecholamines and β2-AR agonists on the expression of intercellular adhesion molecule (ICAM)-1, B7.1, B7.2, CD40, and CD40 ligand (CD40L) in human mixed lymphocyte reaction (MLR) and in an in vitro model of acute rejection in the presence or absence of IL-18. Methods. ICAM-1, B7.1 B7.2, CD40, and CD40L expression on monocytes was measured by flow cytometry, and the production of interferon (IFN)-γ and IL-12 was determined by enzyme-linked immunosorbent assay. Lymphocytes proliferation in MLR was measured by [ 3H]-thymidine uptake. The relevant AR subtypes were characterized using subtype-selective agonists and antagonists. Results. β2-AR agonists inhibited the expression of ICAM-1 and CD40 during MLR in the absence of IL-18. Among IL-18-induced expression of ICAM-1, B7.1, B7.2, CD40, and CD40L, β2-AR agonists inhibited ICAM-1 and CD40 expression. β2-AR agonists prevented the production of IFN-γ and IL-12 in the presence of IL-18 but had no effect in the absence of IL-18. β2-AR agonists inhibited lymphocyte proliferation in IL-18-treated MLR. Conclusions. We found that β2-AR agonists strongly inhibited the expression of ICAM-1 and CD40, irrespective of the presence or absence of IL-18, which is different from that of histamine and prostaglandin E2.

UR - http://www.scopus.com/inward/record.url?scp=0742287319&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0742287319&partnerID=8YFLogxK

U2 - 10.1097/01.TP.0000101517.48541.7B

DO - 10.1097/01.TP.0000101517.48541.7B

M3 - Article

C2 - 14742996

AN - SCOPUS:0742287319

VL - 77

SP - 293

EP - 301

JO - Transplantation

JF - Transplantation

SN - 0041-1337

IS - 2

ER -