α1-acid glycoprotein suppresses rat acute inflammatory paw edema through the inhibition of neutrophils activation and prostaglandin E2 generation

Kazuaki Matsumoto, Koji Nishi, Mari Kikuchi, Daisuke Kadowaki, Yoshiko Tokutomi, Naofumi Tokutomi, Katsuhide Nishi, Ayaka Suenaga, Masaki Otagiri

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

α1-Acid glycoprotein (AGP) is an acute phase protein. Whereas the expression of AGP in an inflammatory state is enhanced by inflammatory cytokines including interleukin-1, 6 (IL-1 and IL-6), and tumor necrosis factor-α (TNF-α), the biological significance of AGP remains unclear. In the current study, the anti-inflammatory effect of AGP on the acute inflammatory state was examined in vivo and in vitro. AGP suppressed carrageenan-, dextran- and kaolin-induced paw edema and vascular permeability in rat. These results suggest that both initial inflammatory mediators (serotonin and histamine) and later inflammatory mediators (prostaglandin and bradykinin) are involved in the anti-inflammatory effects of AGP. In fact, prostaglandin E2 (PGE 2) generation in plasma was significantly inhibited by AGP. Moreover, AGP inhibited the migration of neutrophils treated with N-formyl-methionyl- leucyl-phenylalanine (fMLP) through membrane filter. In addition, AGP significantly suppressed superoxide generation from neutrophils that has been treated with fMLP or phorbol 12-myristate 13-acetate. These results imply that the anti-inflammatory effect of AGP may involve the inhibition of neutrophils migration. The data obtained in this study support a scenario in which an increase in AGP concentration in pathological conditions suppresses inflammation reactions induced by autacoids and neutrophils activities and that AGP plays an important role in the maintenance in the body.

Original languageEnglish
Pages (from-to)1226-1230
Number of pages5
JournalBiological and Pharmaceutical Bulletin
Volume30
Issue number7
DOIs
Publication statusPublished - 2007 Jul
Externally publishedYes

Fingerprint

Neutrophil Activation
Dinoprostone
Edema
Glycoproteins
Acids
Neutrophils
Anti-Inflammatory Agents
Interleukin-1
Interleukin-6
Autacoids
methionyl-leucyl-phenylalanine
N-Formylmethionine Leucyl-Phenylalanine
Kaolin
Acute-Phase Proteins
Carrageenan
Capillary Permeability
Bradykinin
Dextrans
Superoxides
Histamine

Keywords

  • α-acid glycoprotein
  • Neutrophil
  • Paw edema
  • Prostaglandin E

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

α1-acid glycoprotein suppresses rat acute inflammatory paw edema through the inhibition of neutrophils activation and prostaglandin E2 generation. / Matsumoto, Kazuaki; Nishi, Koji; Kikuchi, Mari; Kadowaki, Daisuke; Tokutomi, Yoshiko; Tokutomi, Naofumi; Nishi, Katsuhide; Suenaga, Ayaka; Otagiri, Masaki.

In: Biological and Pharmaceutical Bulletin, Vol. 30, No. 7, 07.2007, p. 1226-1230.

Research output: Contribution to journalArticle

Matsumoto, Kazuaki ; Nishi, Koji ; Kikuchi, Mari ; Kadowaki, Daisuke ; Tokutomi, Yoshiko ; Tokutomi, Naofumi ; Nishi, Katsuhide ; Suenaga, Ayaka ; Otagiri, Masaki. / α1-acid glycoprotein suppresses rat acute inflammatory paw edema through the inhibition of neutrophils activation and prostaglandin E2 generation. In: Biological and Pharmaceutical Bulletin. 2007 ; Vol. 30, No. 7. pp. 1226-1230.
@article{d195ebe35d7341ca836a70e636c9c944,
title = "α1-acid glycoprotein suppresses rat acute inflammatory paw edema through the inhibition of neutrophils activation and prostaglandin E2 generation",
abstract = "α1-Acid glycoprotein (AGP) is an acute phase protein. Whereas the expression of AGP in an inflammatory state is enhanced by inflammatory cytokines including interleukin-1, 6 (IL-1 and IL-6), and tumor necrosis factor-α (TNF-α), the biological significance of AGP remains unclear. In the current study, the anti-inflammatory effect of AGP on the acute inflammatory state was examined in vivo and in vitro. AGP suppressed carrageenan-, dextran- and kaolin-induced paw edema and vascular permeability in rat. These results suggest that both initial inflammatory mediators (serotonin and histamine) and later inflammatory mediators (prostaglandin and bradykinin) are involved in the anti-inflammatory effects of AGP. In fact, prostaglandin E2 (PGE 2) generation in plasma was significantly inhibited by AGP. Moreover, AGP inhibited the migration of neutrophils treated with N-formyl-methionyl- leucyl-phenylalanine (fMLP) through membrane filter. In addition, AGP significantly suppressed superoxide generation from neutrophils that has been treated with fMLP or phorbol 12-myristate 13-acetate. These results imply that the anti-inflammatory effect of AGP may involve the inhibition of neutrophils migration. The data obtained in this study support a scenario in which an increase in AGP concentration in pathological conditions suppresses inflammation reactions induced by autacoids and neutrophils activities and that AGP plays an important role in the maintenance in the body.",
keywords = "α-acid glycoprotein, Neutrophil, Paw edema, Prostaglandin E",
author = "Kazuaki Matsumoto and Koji Nishi and Mari Kikuchi and Daisuke Kadowaki and Yoshiko Tokutomi and Naofumi Tokutomi and Katsuhide Nishi and Ayaka Suenaga and Masaki Otagiri",
year = "2007",
month = "7",
doi = "10.1248/bpb.30.1226",
language = "English",
volume = "30",
pages = "1226--1230",
journal = "Biological and Pharmaceutical Bulletin",
issn = "0918-6158",
publisher = "Pharmaceutical Society of Japan",
number = "7",

}

TY - JOUR

T1 - α1-acid glycoprotein suppresses rat acute inflammatory paw edema through the inhibition of neutrophils activation and prostaglandin E2 generation

AU - Matsumoto, Kazuaki

AU - Nishi, Koji

AU - Kikuchi, Mari

AU - Kadowaki, Daisuke

AU - Tokutomi, Yoshiko

AU - Tokutomi, Naofumi

AU - Nishi, Katsuhide

AU - Suenaga, Ayaka

AU - Otagiri, Masaki

PY - 2007/7

Y1 - 2007/7

N2 - α1-Acid glycoprotein (AGP) is an acute phase protein. Whereas the expression of AGP in an inflammatory state is enhanced by inflammatory cytokines including interleukin-1, 6 (IL-1 and IL-6), and tumor necrosis factor-α (TNF-α), the biological significance of AGP remains unclear. In the current study, the anti-inflammatory effect of AGP on the acute inflammatory state was examined in vivo and in vitro. AGP suppressed carrageenan-, dextran- and kaolin-induced paw edema and vascular permeability in rat. These results suggest that both initial inflammatory mediators (serotonin and histamine) and later inflammatory mediators (prostaglandin and bradykinin) are involved in the anti-inflammatory effects of AGP. In fact, prostaglandin E2 (PGE 2) generation in plasma was significantly inhibited by AGP. Moreover, AGP inhibited the migration of neutrophils treated with N-formyl-methionyl- leucyl-phenylalanine (fMLP) through membrane filter. In addition, AGP significantly suppressed superoxide generation from neutrophils that has been treated with fMLP or phorbol 12-myristate 13-acetate. These results imply that the anti-inflammatory effect of AGP may involve the inhibition of neutrophils migration. The data obtained in this study support a scenario in which an increase in AGP concentration in pathological conditions suppresses inflammation reactions induced by autacoids and neutrophils activities and that AGP plays an important role in the maintenance in the body.

AB - α1-Acid glycoprotein (AGP) is an acute phase protein. Whereas the expression of AGP in an inflammatory state is enhanced by inflammatory cytokines including interleukin-1, 6 (IL-1 and IL-6), and tumor necrosis factor-α (TNF-α), the biological significance of AGP remains unclear. In the current study, the anti-inflammatory effect of AGP on the acute inflammatory state was examined in vivo and in vitro. AGP suppressed carrageenan-, dextran- and kaolin-induced paw edema and vascular permeability in rat. These results suggest that both initial inflammatory mediators (serotonin and histamine) and later inflammatory mediators (prostaglandin and bradykinin) are involved in the anti-inflammatory effects of AGP. In fact, prostaglandin E2 (PGE 2) generation in plasma was significantly inhibited by AGP. Moreover, AGP inhibited the migration of neutrophils treated with N-formyl-methionyl- leucyl-phenylalanine (fMLP) through membrane filter. In addition, AGP significantly suppressed superoxide generation from neutrophils that has been treated with fMLP or phorbol 12-myristate 13-acetate. These results imply that the anti-inflammatory effect of AGP may involve the inhibition of neutrophils migration. The data obtained in this study support a scenario in which an increase in AGP concentration in pathological conditions suppresses inflammation reactions induced by autacoids and neutrophils activities and that AGP plays an important role in the maintenance in the body.

KW - α-acid glycoprotein

KW - Neutrophil

KW - Paw edema

KW - Prostaglandin E

UR - http://www.scopus.com/inward/record.url?scp=34447132199&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34447132199&partnerID=8YFLogxK

U2 - 10.1248/bpb.30.1226

DO - 10.1248/bpb.30.1226

M3 - Article

C2 - 17603158

AN - SCOPUS:34447132199

VL - 30

SP - 1226

EP - 1230

JO - Biological and Pharmaceutical Bulletin

JF - Biological and Pharmaceutical Bulletin

SN - 0918-6158

IS - 7

ER -