Analysis of the gene expression profile activated by the CC chemokine ligand 5/RANTES and by lipopolysaccharide in human monocytes

J Immunol. 2002 Apr 1;168(7):3557-62. doi: 10.4049/jimmunol.168.7.3557.

Abstract

The gene expression profile induced by the CC chemokine ligand (CCL) 5/RANTES in human monocytes was examined using the oligonucleotide array technology. Of 5600 transcripts examined, 42 were consistently induced by CCL5, and none were suppressed. Chemokine-inducible transcripts could be clustered in functional groups, including selected cytokines and receptors (e.g., IL-1beta, CCL2/monocyte chemotactic protein-1, and the CCL5 receptor CCR1) and molecules involved in extracellular matrix recognition and digestion (e.g., CD44 splice transcripts, urokinase-type plasminogen activator receptor, matrix metalloprotease (MMP)-9, and MMP-19). Transcript expression, confirmed by quantitative real-time PCR analysis for selected genes, was associated with protein induction for some (e.g., CCL2), but not all (e.g., IL-1beta), transcripts examined. The chemokine-induced gene profile was distinct from that activated by LPS, a prototypic phagocyte activator. Although certain transcripts were stimulated by both agonists (e.g., IL-1beta and CCL2), others were induced only by either LPS (e.g., TNF-alpha and IL-6) or CCL5 (e.g., MMP-19) or were divergently regulated (e.g., CCR1). Thus, CCL5, a prototypic CC inflammatory chemokine, activates a restricted transcriptional program in monocytes distinct from that induced by the prototypic pathogen-derived proinflammatory stimulant LPS. Chemokine-induced chemokines production could represent a novel amplification loop of leukocyte recruitment, while a subset of chemokine-inducible transcripts could be involved in monocyte extravasation and tissue invasion.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Chemokine CCL5 / metabolism
  • Chemokine CCL5 / pharmacology*
  • Chemokines, CC / metabolism*
  • Gene Expression Profiling* / methods
  • Gene Expression Regulation / immunology*
  • Humans
  • Inflammation / genetics
  • Inflammation / immunology
  • Ligands
  • Lipopolysaccharides / pharmacology*
  • Monocytes / immunology*
  • Monocytes / metabolism*
  • RNA, Messenger / biosynthesis
  • Signal Transduction / genetics
  • Signal Transduction / immunology
  • Transcription, Genetic / immunology

Substances

  • Chemokine CCL5
  • Chemokines, CC
  • Ligands
  • Lipopolysaccharides
  • RNA, Messenger