Transforming growth factor-beta1 enhances the secretion of monocyte chemoattractant protein-1 by the IEC-18 intestinal epithelial cell line
Related Experiment Video
Updated: Aug 31, 2026

Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes
Published on: May 31, 2018
Lisa B Matagrano1, Jason A Magida, Dennis W McGee
1Department of Biological Sciences, Binghamton University (SUNY), Binghamton, New York 13902-6000, USA.
Abstract:
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.
More Related Videos
Related Concept Videos
TGF - β Signaling Pathway
Differentiation of Common Myeloid Progenitor Cells
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal
Renewal of Intestinal Stem Cells

