The primary
polyphenol in
green tea extract is the
catechin epigallocatechin gallate (EGCG). Various studies have shown significant suppressive effects of
catechin on mammalian cells, either
tumor or normal cells, including lymphoid cells. Previous studies from this laboratory reported that EGCG has marked suppressive activity on murine macrophages infected with the intracellular bacterium Legionella pneumophila (Lp), an effect mediated by enhanced production of both
tumor necrosis factor-alpha (
TNF-alpha) and
gamma-interferon (IFN-gamma). In the present study, primary murine bone marrow (BM)-derived dendritic cells (DCs), a phagocytic monocytic cell essential for innate immunity to intracellular microorganisms, such as Lp, were stimulated in vitro with the microbial stimulant
lipopolysaccharide (LPS) from gram-negative bacteria, the cell wall component from gram-positive bacteria muramyldipeptide (MDP) or infected with Lp. Production of the T helper cell (Th1)-activating
cytokine,
interleukin-12 (IL-12) and the proinflammatory
cytokine,
tumor necrosis factor-alpha (
TNF-alpha),produced mainly by phagocytic cells and important for antimicrobial immunity, was determined in cell culture supernatants by
enzyme-linked
immunosorbent assay (ELISA). Treatment of the cells with EGCG inhibited, in a dose-dependent manner, production of
IL-12. In contrast, enhanced production of
TNF-alpha occurred in a dose-dependent manner in the DC cultures stimulated with either soluble bacterial product or infected with Lp. Thus, the results of this study show that the EGCG
catechin has a marked effect in modulating production of these immunoregulatory
cytokines in stimulated DCs, which are important for antimicrobial immunity, especially innate immunity. Further studies are necessary to characterize the physiologic function of the effect of EGCG on
TNF-alpha and
IL-12 during Lp
infection, and the mechanisms involved.