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The ability to eliminate Escherichia coli K-12 from the peritoneal cavity in the early stage of infection (48 h) was improved by the pre-administration of an aloe sample to BALB/c mice. Our results suggest that the aloe sample could inhibit infectious diseases by stimulating the host defense mechanism, especially the phagocytic and killing activities of macrophages.

The retention of deoxynivalenol in noodles and bread made from naturally-contaminated flour was examined by a chemical analysis (HPLC) and bioassays. The retention level of deoxynivalenol obtained from both assays was reduced by boiling process, although only the bioassays showed it to have been reduced by baking. This study is the first to estimate the exposure to deoxynivalenol from the consumption of the final products of wheat flour in Japan.

We investigated the change in renal mdr1b mRNA expression in offspring exposed to tributyltin chloride (TBTC) via the placenta and lactation or via lactation, using the real-time reverse transcription-polymerase chain reaction. Pregnant ICR mice were given water containing TBTC (0, 15, and 50 microg/ml) ad libitum from the start of pregnancy to weaning or from parturition to weaning. Exposure via the placenta and lactation significantly reduced the renal mdr1b level in offspring. Exposure to TBTC through the mother might impair the exclusion system of toxic compounds in offspring.

We examined the effect of lactational exposure to tributyltin on innate immunodefenses in the F1 generation using in vivo and in vitro experiments. Pregnant C57BL/6 mice were given drinking water containing 0, 15, or 50 microg/ml of tributyltin chloride (TBTCl) from parturition to weaning. At weaning time, offspring were inoculated with Escherichia coli K-12, and bacterial clearances from the peritoneal cavity and spleen were examined. In vivo infection experiments indicated that bacterial clearance was significantly depressed in offspring breast-fed by dams exposed to 15 microg/ml of TBTCl (15 ppm F1), but not in offspring by dams exposed to 50 microg/ml of TBTCl (50 ppm F1). In vitro functional assays revealed that the killing activity of neutrophils decreased significantly in 15 ppm F1, but not in 50 ppm F1. We suggest that lactational exposure to TBT impairs innate immunodefenses in the F1 generation against non-pathogenic bacterial infection.

We studied the activity of wine against entero-pathogenic bacteria both in vitro and in vivo. The food-borne bacteria were killed in both red and white wine within 30 min. However, the results of a Salmonella infection experiment using mice suggested that wine was not effective in preventing food-borne diseases in vivo.

We investigated the immunological function of cheese whey protein concentrate (CWPC), which is a by-product of cheese production, using mitogenic activity in murine splenocytes as an index. A fraction isolated by gel filtration and anion exchange chromatography of CWPC showed high mitogenic activity, comparable to the activity of lipopolysaccharide (LPS). The fraction was detected as a single band on SDS-PAGE. It contained calcium, inorganic phosphorus, and carbohydrate, indicating the active component to be a glycophosphopeptide (GPP). Since Pronase digestion of GPP did not reduce its mitogenic activity, carbohydrate rather than peptide may be important in the activity. When applied on an anti-beta-caseinophosphopeptide (beta-CPP) antibody affinity column, the GPP was separated into two components, one with affinity to beta-CPP and the other without such affinity. Both the components contained N-linked oligosaccharide chains and had the mitogenic activity. These results demonstrate that cheese whey contains a GPP having strong mitogenic activity.

The preventive effects of glycomacropeptide (GMP) against intestinal infection were investigated, and conjugates of GMP with xylooligosaccharide (XOS) and carboxymethyldextran (CMD) were prepared by the Maillard reaction to enhance the effect of GMP. The binding ability of GMP to intestinal pathogenic bacteria was evaluated by a binding assay with biotinylated bacteria. GMP showed the ability to bind to Salmonella enteritidis and enterohemorrhagic Escherichia coli O157:H7 (EHEC O157). This binding ability was decreased by a sialidase treatment and completely eliminated by periodate oxidation. These results indicate that such carbohydrate moieties as sialic acid in GMP are involved in binding to S. enteritidis and EHEC O157. The preventive effect of GMP on the adhesion of pathogenic bacteria to Caco-2 cells was also investigated. GMP showed an inhibitory effect on the adhesion of EHEC O157 in a dose-dependent manner, although it was not a potent inhibitor of the adhesion of Salmonella infection. However, in the case of Salmonella infection, GMP-XOS and GMP-CMD significantly suppressed IL-8 production which was the index of infection. Our results indicate GMP to be a promising agent for preventing intestinal infection.

The effects of carrageenans (CGNs) on the host defense mechanisms of macrophages against Salmonella infection were examined in vitro by using macrophage-like J774.1 cells. Iota-CGN reduced the Salmonella-binding and phagocytotic activities of J774.1 cells, but it increased the killing activity of the cells. Kappa-CGN increased the binding activity, but reduced the killing ability. CGNs would affect the host defense mechanisms by modulating the macrophage functions.

We studied the effect of lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the susceptibility to Listeria infection of offspring in C57BL /6NCji mice. The offspring were nursed by TCDD-treated dams and exposed to TCDD from birth to weaning via milk. The exposure had little effect on the weights of immune organs and the spleen or the thymus cell population in the dams and offspring, but it enhanced the production of tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma) in the serum after Listeria infection. The clearance of Listeria monocytogenes from the spleen was impaired in the off-spring. These results suggest that the exposure to TCDD of the offspring via milk disrupted the host resistance of the offspring, even though the main immune parameters were unchanged.