Macrophages (MΦs), the major population of tissue-resident mononuclear phagocytes, play key roles in bacterial recognition and elimination as well as in polarization of innate and adaptive immunities. Since the intestinal mucosa of the gut is always exposed to numerous enteric bacteria including both pathogenic and non-pathogenic bacteria, it is considered that the gut may possess regulatory mechanisms preventing excessive inflammatory responses. On the other hand, it has become evident that abnormal innate immune responses to enteric bacteria are responsible for the pathogenesis of IBD. It became evident by our present study that intestinal MΦs from wild-type mice produced large amounts of IL-10 but failed to produce IL-12 and IL-23 in response to enteric bacteria. In contrast, in IL-10^-/-mice, intestinal MΦs differentiated into abnormal phenotypes under an IL-10 deficient environment, and produced abnormally large amounts of IL-12 and IL-23 in response to enteric bacteria. These results suggest that intestinal MΦs act as anti-inflammatory MΦs, and suppress excess inflammation induced by enteric bacteria in the normal state. In IL-10^-/-mice, however, intestinal MΦs differentiated into abnormal phenotypes, and enteric bacteria recognition by these abnormally differentiated subsets of intestinal MΦ may lead to Th1-dominant colitis via IL-12 and IL-23 hyperproduction.

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Helicobacter pylori is a Gram-negative helical bacterium which colonizes gastric mucosa persistently. H. pylori induces acute and chronic gastritis, and acts as recurrence factor or healing-delaying factor for peptic ulcer diseases. In addition, it is implicated that H. pylori infection has been associated with malignant diseases such as gastric cancer and gastric MALT lymphoma. Virulence factors of H. pylori are grouped into bacterial and host virulence factors. Urease, adhesin, VacA cytotoxin, CagA, cagPAI, OipA, NapA, heat-shock protein etc have been reported as bacterial virulence factors. Translocation of CagA into a host cell through the Type IV secretion system induces considerable changes in cellular function, and plays an important role in pathogenesis following H. pylori infection. Cytokines (TNFα, IL-6, IL-8 etc) produced by gastric epithelial cells and immune cells, oxyradicals and nitiric oxide (NO) have been reported as host virulence factors. In addition, the association of H. pylori with extra-gastroduodenal diseases such as idiopathic thrombocytopenic purpura, chronic urticaria, coronary artery diseases etc.) has been reported, and improvement of the above diseases was reported after H. pylori eradication therapy.

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Food poisoning caused by enterohemorrhagic Escherichia coli (EHEC) has occurred frequently in schools and homes for the elderly since 1990. Drinking tea is popular in Japan and the antibacterial effect of catechin has been reported. We studied the inhibitory effect of tea and catechin drinks on growth and vero toxin (VT) production in EHEC O 157. Growth of each strain of E. coli was inhibited by a catechin-containing medium. Stronger inhibitory effects were recognized in green tea medium and black tea medium, which contained more catechin (epigallocatechin gallate and epicatechin gallate) possessing galloyl moiety. In MV1184 and HK, stronger inhibitory effects were recognized in green tea medium and coarse tea medium, which contained more caffeine. These data support the possibility that factor other than catechin have an inhibitory effect on bacterial growth. Three bacteria were cultivated in LB broth medium and the number of colonies was measured. The growth of EDL931 was fastest followed by HK; MV1184 showed the slowest growth. HK and EDL931 produced vero toxin and its production was inhibited or prevented in each medium (black tea medium, two kinds of green tea medium and coarse tea medium). These data supports the high possibility that food poisoning is prevented by drinking tea.

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