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Updated: Jun 18, 2026
Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
Published on: October 17, 2017
Epigallocatechin gallate reduces human monocyte mobility and adhesion in vitro
Esther Melgarejo1, Miguel Angel Medina, Francisca Sánchez-Jiménez
1Departamento de Biología Molecular y Bioquímica, Facultad de Ciencias, Universidad de Málaga, and CIBER de Enfermedades Raras (CIBERER), Málaga, Spain.
Background And Purpose:
Monocytes/macrophages are an important population of immune inflammatory cells that have diverse effector functions in which their mobility and adhesion play a very relevant role. Epigallocatechin gallate (EGCG), a major component of green tea, has been reported to have anti-allergic and anti-inflammatory activities, but its effects on monocytes remain to be determined. Here we investigated the effects of EGCG on the migration and adhesion of monocytes.
Experimental Approach:
We used a human monocyte cell line (THP-1) to analyse the effects of treatment with EGCG under non-cytotoxic conditions on the expression levels of the monocyte chemotactic protein-1 (MCP-1) and of the MCP-1 receptor (CCR2) and on the activation of beta1 integrin. A functional validation was carried out by evaluating the inhibitory effect of EGCG on monocyte adhesiveness and migration in vitro.
Key Results:
Treatment of THP-1 cells with EGCG decreased MCP-1 and CCR2 gene expression, together with MCP-1 secretion and CCR2 expression at the cell surface. EGCG also inhibited beta1 integrin activation. The effects on these molecular targets were in agreement with the EGCG-induced inhibition of THP-1 migration in response to MCP-1 and adhesion to fibronectin.
Conclusions And Implications:
Under our experimental conditions, EGCG treatment inhibited the migration and adhesion of monocytes. These inhibitory effects of EGCG on monocyte function should be considered as a promising new anti-inflammatory response with a potential therapeutic role in the treatment of inflammation-dependent diseases.
