Transforming growth factor-beta1 enhances the secretion of monocyte chemoattractant protein-1 by the IEC-18 intestinal epithelial cell line.
Intestinal epithelial cells (IEC) are known to produce monocyte chemoattractant protein-1 (MCP-1). However, MCP-1 production, as with many other cytokines, can be regulated by a network of cytokines present in the environment of the IEC. Both IEC and inflammatory cells have been shown to produce transforming growth factor-beta (TGF-beta), and the regulatory effect of this cytokine on MCP-1 secretion by IEC has not been determined. Using the IEC-18 cell line, we have found that TGF-beta1 alone induced the secretion of high levels of MCP-1. Treatment with TGF-beta1 also enhanced the levels of MCP-1 messenger ribonucleic acid. However, costimulation of the cells with TGF-beta1 and interleukin-1beta (IL-1beta) resulted in significant, but less than additive, increases in MCP-1 secretion. Finally, the enhancing effect of TGF-beta1 on MCP-1 secretion was not due to IL-6. These results suggest that TGF-beta1 from IEC or inflammatory cells may significantly enhance the secretion of MCP-1 by IEC and play an important role in inflamed mucosal tissues.
D000818:Animals; D018932:Chemokine CCL2 / Q000378:metabolism*; D007375:Interleukin-1 / Q000494:pharmacology; D007413:Intestinal Mucosa / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D007700:Kinetics; D051381:Rats; D016212:Transforming Growth Factor beta / Q000494:pharmacology*; D053773:Transforming Growth Factor beta1
D018932:Chemokine CCL2; D007375:Interleukin-1; C508962:Tgfb1 protein, rat; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1