Published January 9, 2009 | Version v1
Journal article

Adiponectin stimulates IL-8 production by rheumatoid synovial fibroblasts

  • 1. Department of Immunology, Toho University School of Medicine, Tokyo (Japan)
  • 2. Division of Rheumatology, Department of Internal Medicine, Toho University School of Medicine, 6-11-1 Omori-Nishi, Ota-ku, Tokyo 143-8541 (Japan)
  • 3. Department of Orthopaedic Surgery, Toho University School of Medicine, Tokyo (Japan)

Description

The adipokines are linked not only to metabolic regulation, but also to immune responses. Adiponectin, but not leptin or resistin induced interleukin-8 production from rheumatoid synovial fibroblasts (RSF). The culture supernatant of RSF treated with adiponectin induced chemotaxis, although adiponectin itself had no such effect. Addition of antibody against adiponectin, and inhibition of adiponectin receptor gene decreased adiponectin-induced IL-8 production. Nuclear translocation of nuclear factor-kappa B was increased by adiponectin. The induction of interleukin-8 was inhibited by mitogen-activated protein kinase inhibitors. These findings suggest that adiponectin contributes to the pathogenesis of rheumatoid arthritis.

Availability note (English)

Available from http://dx.doi.org/10.1016/j.bbrc.2008.11.017

Additional details

Identifiers

DOI
10.1016/j.bbrc.2008.11.017;
PII
S0006-291X(08)02201-8;

Publishing Information

Journal Title
Biochemical and Biophysical Research Communications
Journal Volume
378
Journal Issue
2
Journal Page Range
p. 218-223
ISSN
0006-291X
CODEN
BBRCA9

INIS

Country of Publication
United States
Country of Input or Organization
International Atomic Energy Agency (IAEA)
INIS RN
41006417
Subject category
S60: APPLIED LIFE SCIENCES;
Descriptors DEI
ANTIBODIES; FIBROBLASTS; GENES; INFLAMMATION; INHIBITION; LEPTIN; PATHOGENESIS; RHEUMATIC DISEASES
Descriptors DEC
ANIMAL CELLS; CONNECTIVE TISSUE CELLS; HORMONES; ORGANIC COMPOUNDS; PATHOLOGICAL CHANGES; PEPTIDE HORMONES; PEPTIDES; POLYPEPTIDES; PROTEINS; SOMATIC CELLS; SYMPTOMS

Optional Information

Copyright
Copyright (c) 2008 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.