The use of such substances to prevent or moderate infectious diseases is a cornerstone of traditional Chinese medicine and also alternative medicine in Western countries. In this regard, there has been increased interest in prophylactic treatment to prevent or ameliorate clinical infection or re-infection by opportunistic microbes which cause chronic disease, including gastritis due to H. pylori. Such substances are often derived from extracts of plants considered medicinal. In particular, many recent studies have been reported with green tea extracts, especially polyphenols such as catechins, which are the active component of tea (Mabe et al., 1999; Yamaguchi et al., 2002). Although many catechins are present in tea, the most common is epigallocatechin gallate (EGCG), which accounts for much of the in vitro antimicrobial activity of tea first reported in biomedical journals a century ago. Catechins (also known as flavanols) are group of polyphenols found in many natural plant-derived products, particularly green tea. The four major catechins are EGCG, epigallocatechin (EGC), epicatechin gallate (ECG), and epicatechin (EC) (Yang et al., 2002). The typical percentage of individual catechins in green tea extracts is 10-15% ECGC, 2-3% ECG, 2% EC and 2-3% EGC (Suganuma et al., 1999). Thus, EGCG is the major catechin in green tea, and also accounts for most of the reported biological effects of green tea, especially antitumor effects (Morre etal., 2003).
Demonstrable antimicrobial activity by EGCG has been reported against a wide variety of microorganisms, including Chlamydia trachomatis, Chlamydia pneumoniae (Yamazaki et al., 2003) and Helicobacter pylori (Yanagawa et al., 2003). EGCG has also been considered to have an antiviral activity, as shown by its potent effect in vitro in HIV-1 (Yamaguchi et al., 2002). Furthermore, a number of laboratories reported that a variety of nonspecific cytokines induced by EGCG have direct antimicrobia1 activity against various microorganisms, including common extracellular bacteria like staphylococci, streptococci or even fungi. EGCG treatment of Lp-infected macrophages resulted in enhanced production of TNFa, which markedly inhibited Lp virulence activity. Specifically, a report published in 2002 showed that the growth of Lp in permissive macrophages was selectively inhibited by small amounts of EGCG, the major active green tea catechin. This antimicrobial activity was not due to direct effects on the bacteria itself, since EGCG did not alter Lp growth in the incubation medium, regardless of various Lp concentrations used (Matsunaga et al., 2001a).
Epigallocatechin gallate also rescued permissive macrophages from diminished resistance to Lp infection due to either cigarette smoke condensate or nicotine. Again, the mechanism by which EGCG overcame enhanced susceptibility to infection caused by treatment with these immunosuppressive substances involved, at least in part, upregulation of TNFa, as well as IFN7 production by activated macrophages, since neutralization of these cytokines by monoclonal antibodies markedly abolished the protective effects of EGCG (Matsunaga et al., 2002). IFN7 produced by NK cells has also recently been reported as a key factor in controlling Lp infection in a permissive mouse model (Sporri et al., 2006).
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