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Alliin Allicin Cytokine production Peyer's patch DNA microarray A B S T R A C T The effects of garlic extract and three organosulphur compounds of garlic on intestinal immune responses in mice were investigated. Peyer's patch (PP) cells were isolated from mice orally administered with garlic extracts or one of three organosulphur compounds (alliin, allicin, diallyl disulphide (DADS)). PP cells isolated from mice that had been orally injected with ethanol extract significantly produced interferon (IFN)-c and interleukin (IL)-4. IL-2 production in PP cells was significantly reduced by hot-water and ethanol extracts from garlic. PP cells from mice administered with two organosulphur compounds, alliin or DADS (5 mg/kg/day), could produce IL-2, IFN-c and IL-4, whereas allicin showed moderate activity. The enhancement activity of IL-2 and IFN-c productions in PP cells by DADS was higher than those obtained by administration of alliin or allicin. Comprehensive analyses of genetic profiles in PP tissue from mice administered with ethanolic extracts, allicin or alliin revealed that oral administration of samples increased 68-144 genes and decreased 50-52 genes by P1.8-fold. Analyses of clustering profiles of microarrays indicated that ethanol extract and alliin upregulated the expression of IFN-c. These data showed that garlic and its organosulphur compounds stimulate de novo IFN-c biosynthesis in PP cells, thereby promoting ileal immune responses.

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The SOS response is induced upon DNA damage and the inhibition of Z ring formation by the product of the sulA gene, which is one of the LexA-regulated genes, allows time for repair of damaged DNA. On the other hand, severely DNA-damaged cells are eliminated from cell populations. Overexpression of sulA leads to cell lysis, suggesting SulA eliminates cells with unrepaired damaged DNA. Transcriptome analysis revealed that overexpression of sulA leads to up-regulation of numerous genes, including soxS. Deletion of soxS markedly reduced the extent of cell lysis by sulA overexpression and soxS overexpression alone led to cell lysis. Further experiments on the SoxS regulon suggested that LpxC is a main player downstream from SoxS. These findings suggested the SulA-dependent cell lysis (SDCL) cascade as follows: SulA→SoxS→LpxC. Other tests showed that the SDCL cascade pathway does not overlap with the apoptosis-like and mazEF cell death pathways.