Differential regulation of C-C chemokines during fibroblast-monocyte interactions: adhesion vs. inflammatory cytokine pathways
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 of information relating to the maintenance of chronic fibrotic diseases . Using a lung fibroblast...
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| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
1998-01-01
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| Series: | Mediators of Inflammation |
| Subjects: | |
| Online Access: | http://dx.doi.org/10.1080/09629359890956 |
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| Summary: | 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 of
information relating to the maintenance of chronic fibrotic diseases . Using a lung fibroblast line and
enriched monocyte populations , we have investigated the activational events which contribute to the production
of two C-C chemokines , macrophage inflammatory protein-1 alpha (MIP-1α ) and monocyte
chemoattractant 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, when
isolated 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 derived
from monocytes and MCP-1 from both cell populations. To examine the molecules which wer erequired
for 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 decreased
MCP-1 production during the co-culture . These data indicate that fibroblast–monocyte inte ractions
induce chemokine production through different mechanisms and a combination of these responses
may contribute to the maintenance of the mononuclear cell accumulation during diseaseprogression. |
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| ISSN: | 0962-9351 1466-1861 |