• Medientyp: E-Artikel
  • Titel: Differential regulation of C‐C chemokines during fibroblast‐monocyte interactions: adhesion vs. inflammatory cytokine pathways
  • Beteiligte: Zickus, C.; Kunkel, S. L.; Simpson, K.; Evanoff, H.; Glass, M.; Strieter, R. M.; Lukacs, N. W.
  • Erschienen: Wiley, 1998
  • Erschienen in: Mediators of Inflammation, 7 (1998) 4, Seite 269-274
  • Sprache: Englisch
  • DOI: 10.1080/09629359890956
  • ISSN: 0962-9351; 1466-1861
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  • Anmerkungen:
  • Beschreibung: The cell‐to‐ce ll interactions during chronic inflammatory diseases likely contribute to leukocyte accumulation leading to increased pathology and organ dys ‐function. In particular, there is a paucity ofinformation relating to the maintenance of chronic fibrotic diseases . Using a lung fibroblast line andenriched monocyte populations , we have investigated the activational events which contribute to the productionof two C‐C chemokines , macrophage inflammatory protein‐1 alpha (MIP‐1α ) and monocytechemoattractant protein‐1 (MCP‐1), during fibroblas tmonocyte interactions . Neither the fibroblast cell line(16 lu) nor isolated monocytes alone produced significant levels of MIP‐1α or MCP‐1. However, whenisolated monocytes were layered onto 16 lu fibroblas tmonolayers as ignificant increase in MIP‐1α and MCP‐1 production was observed. The use of fixed cell populations indicated that the MIP‐1α was derivedfrom monocytes and MCP‐1 from both cell populations. To examine the molecules which wer erequiredfor chemokine production during the interaction, specific antibodies were used in the co‐cultures .Blocking β3‐integrin interactions s ignificantly inhibited MIP‐1α production. In contrast, beta‐integr in interactions had no effect on the MCP‐1 production, while, neutralization of TNF significantly decreasedMCP‐1 production during the co‐culture . These data indicate that fibroblast–monocyte inte ractionsinduce chemokine production through different mechanisms and a combination of these responsesmay contribute to the maintenance of the mononuclear cell accumulation during diseaseprogression.
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