Abstract
In this study, we explored the potential beneficial effects of green tea extract (GTE) in a pathogenic Escherichia coli (F18:LT:STa:Stx2e)-induced colitis model. The GTE was standardized with catechin and epigallocatechin-3-gallate content using chromatography analysis. Ten consecutive days of GTE (500 and 1000 mg/kg) oral administration was followed by 3 days of a pathogenic E. coli challenge (1 × 109 CFU/mL). In vitro antibacterial analysis showed that GTE successfully inhibited the growth of pathogenic E. coli, demonstrating over a 3-fold reduction under time- and concentration-dependent conditions. The in vivo antibacterial effect of GTE was confirmed, with an inhibition rate of approximately 90% when compared to that of the E. coli alone group. GTE treatment improved pathogenic E. coli-induced intestinal injury with well-preserved epithelial linings and villi. In addition, the increased expression of annexin A1 in GTE-treated jejunum tissue was detected, which was accompanied by suppressed inflammation-related signal expression, including TNFA, COX-2, and iNOS. Moreover, proliferation-related signals such as PCNA, CD44, and Ki-67 were enhanced in the GTE group compared to those in the E. coli alone group. Taken together, these results indicate that GTE has an antibacterial activity against pathogenic E. coli and ameliorates pathogenic E. coli-induced intestinal damage by modulating inflammation and epithelial cell proliferation.
Highlights
Escherichia coli (E. coli) is normally found in intestinal flora and typically colonizes the gastrointestinal tract
Previous studies categorized pathogenic E. coli by its pathotype, and, among the groups, enteropathogenic E. coli, enterohemorrhagic E. coli, and enterotoxigenic E. coli (ETEC) were reported to cause disease in both humans and animals using many of the common virulence factors [4]
We described the biological effects of standardized green tea extract (GTE) administration against pathogenic E. coli-induced colitis in mice
Summary
Escherichia coli (E. coli) is normally found in intestinal flora and typically colonizes the gastrointestinal tract. E. coli presents special pathogenic factors that were reported to cause a wide spectrum of infectious diseases [2]. E. coli is a common cause of diarrheal disease worldwide and it is estimated that 200 million people are affected by it every day. Previous studies categorized pathogenic E. coli by its pathotype, and, among the groups, enteropathogenic E. coli, enterohemorrhagic E. coli, and enterotoxigenic E. coli (ETEC) were reported to cause disease in both humans and animals using many of the common virulence factors [4]. Pathogenic E. coli adhere to specific host cells with adhesins, called fimbriae, to colonize and secrete various toxins such as the Shiga toxin (Stx), as well as heat-labile (LT) and heat-stable (ST) toxins to compromise cell function [5]. Pathogenic E. coli-induced colonic damage is accompanied with intense inflammation [6]. Lipopolysaccharides (LPS) and flagella in E. coli trigger a potent inflammatory cytokine cascade and stimulate annexin A1 (Anex1) expression, which is an anti-inflammatory protein that inhibits inflammatory cell transmigration and phospholipase A2 activation [4,7]
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