Anti-infective properties of epigallocatechin-3-gallate (EGCG), a component of green tea - PubMed (original) (raw)

Review

Anti-infective properties of epigallocatechin-3-gallate (EGCG), a component of green tea

J Steinmann et al. Br J Pharmacol. 2013 Mar.

Abstract

The consumption of green tea (Camellia sinensis) has been shown to have many physiological and pharmacological health benefits. In the past two decades several studies have reported that epigallocatechin-3-gallate (EGCG), the main constituent of green tea, has anti-infective properties. Antiviral activities of EGCG with different modes of action have been demonstrated on diverse families of viruses, such as Retroviridae, Orthomyxoviridae and Flaviviridae and include important human pathogens like human immunodeficiency virus, influenza A virus and the hepatitis C virus. Furthermore, the molecule interferes with the replication cycle of DNA viruses like hepatitis B virus, herpes simplex virus and adenovirus. Most of these studies demonstrated antiviral properties within physiological concentrations of EGCG in vitro. In contrast, the minimum inhibitory concentrations against bacteria were 10-100-fold higher. Nevertheless, the antibacterial effects of EGCG alone and in combination with different antibiotics have been intensively analysed against a number of bacteria including multidrug-resistant strains such as methicillin-resistant Staphylococcus aureus or Stenotrophomonas maltophilia. Furthermore, the catechin EGCG has antifungal activity against human-pathogenic yeasts like Candida albicans. Although the mechanistic effects of EGCG are not fully understood, there are results indicating that EGCG binds to lipid membranes and affects the folic acid metabolism of bacteria and fungi by inhibiting the cytoplasmic enzyme dihydrofolate reductase. This review summarizes the current knowledge and future perspectives on the antibacterial, antifungal and antiviral effects of the green tea constituent EGCG.

© 2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society.

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Figures

Figure 1

Figure 1

Chemical structure of the four major catechins in green tea.

Figure 2

Figure 2

HCV entry into human hepatocytes and interference by EGCG. Cell entry involves an interaction between the extracellular virion that is associated with lipoproteins and several receptors on the host cell membrane. These include scavenger receptor type B class 1 (SR-BI), epidermal growth factor receptor (EGF-R), CD81, claudin 1 (CLDN1), ocludin (OCLN), Niemann-PickC1-like 1 (NPC1L1) and possibly low-density lipoprotein receptor (LDL-R). It has been suggested that the lipoprotein receptors SR-BI and LDL-R act before CD81 and the tight junction components CLDN1 and OCLN. These interactions induce travelling of the virus-receptor complex along the cell surface from the basolateral (blood-side) surface of the hepatic epithelium where LDL-R, SR-BI and CD81 are localized to the tight junction region, where CLDN1 and OCLN are encountered. These events stimulated by virion-mediated activation of receptor tyrosine kinase signalling like EGF-R result in clathrin-dependent endocytosis of the virion. Acidification of the endosome triggers a fusion peptide activity within the glycoproteins E1 or E2, the viral envelope fuses with the endosomal membrane and the nucleocapsid is released into the cytosol. EGCG is suggested to act on the virus particle and inhibits virus entry by impairing virus binding to the cell surface.

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