Papers

Dec, 2000

Neutrophil infiltration as a crucial step for monocyte chemoattractant protein (MCP)-1 to attract monocytes in lipopolysaccharide-induced arthritis in rabbits

INFLAMMATION RESEARCH
  • S Miyazaki
  • ,
  • A Matsukawa
  • ,
  • S Ohkawara
  • ,
  • K Takagi
  • ,
  • M Yoshinaga

Volume
49
Number
12
First page
673
Last page
678
Language
English
Publishing type
Research paper (scientific journal)
DOI
10.1007/s000110050645
Publisher
BIRKHAUSER VERLAG AG

Objective and Design: To evaluate the mechanism whereby monocyte chemoattractant protein (MCP)-1 attracts monocytes in vivo.
Subjects: New Zealand white rabbits (175 rabbits) were used.
Treatment: LPS, MCP-1 or IL-8 was injected into knee joints. Antibodies against various cytokines or IL-1 receptor antagonist were injected to neutralize cytokine activities.
Methods: The numbers of leukocyte populations, levels of cytokines in joints were estimated.
Results: Partial inhibition of neutrophil influx with anti-IL-8 IgG (10 mug) suppressed LPS-induced macrophage influx by 43 +/- 8.5% (p<0.05) without affecting the MCP-I level. Intraarticular injection of MCP-1 (1-30 <mu>g) induced macrophage influx. The event was accompanied by a small number of neutrophils in an early phase. Go-injection of IL-8 (1.0 mug) enhanced the MCP-1-induced macrophage infiltration (p<0.01). In neutrophil-depleted rabbits, LPS failed to induce macrophage influx even though the MCP-1 level was maintained, and macrophage influx following exogenously administered MCP-1 was also dramatically inhibited.
Conclusions: Early events associated with neutrophil infiltration appear to be important for MCP-1 to induce a later macrophage influx in LPS-arthritis.

Link information
DOI
https://doi.org/10.1007/s000110050645
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000166814100004&DestApp=WOS_CPL
ID information
  • DOI : 10.1007/s000110050645
  • ISSN : 1023-3830
  • Web of Science ID : WOS:000166814100004

Export
BibTeX RIS