We previously observed that gut colonization by Candida albicans promoted serum antibody response to orally administered ovalbumin in mice. We therefore postulated that C. albicans affects oral tolerance induction. The present study tested this idea. BALB/c mice were intragastrically administered with either C. albicans (1 × 107) or vehicle, and the colonization was confirmed by weekly fecal cultures. Mice were further divided into two subgroups and intragastrically administered with either ovalbumin (20 mg) or vehicle for five consecutive days. Thereafter, all mice were intraperitoneally immunized with ovalbumin in alum. In mice without C. albicans inoculation, ovalbumin feeding prior to immunization significantly suppressed the increase in ovalbumin-specific IgE, IgG1 and IgG2a in sera, suggesting oral tolerance induction. In C. albicans-inoculated mice, however, the antibody levels were the same between ovalbumin- and vehicle-fed mice. In contrast, ovalbumin feeding significantly suppressed cellular immune responses, as evidenced by reduced proliferation of splenocytes restimulated by ovalbumin ex vivo, in both C. albicans-inoculated and uninoculated mice. Ex vivo supplementation with neither heat-killed C. albicans nor the culture supernatant of C. albicans enhanced the production of ovalbumin-specific IgG1 in splenocytes restimulated by the antigen. These results suggest that gut colonization by C. albicans inhibits the induction of humoral immune tolerance to dietary antigen in mice, whereas C. albicans may not directly promote antibody production. We therefore propose that C. albicans gut colonization could be a risk factor for triggering food allergy in susceptible individuals.
The present study tested the persistence of orally administered bacteria in the gut of suckling mice. We used three bacterial strains: one strain of Lactobacillus johnsonii (designated strain Ms1) that was previously isolated from the mouse stomach, and two strains of L. plantarum, (strain No. 14 and JCM 1149T). We detected L. johnsonii Ms1, but neither strain of L. plantarum, in the gut 7 days after administration when the organisms were administered on days 0, 1, 3 or 7 of neonatal life. None of the strains was detected in the gut 7 days after the administration on days 14 or 28 of neonatal life. L. johnsonii Ms1 and L. plantarum JCM 1149T exhibited similar levels of in vitro association with gut tissues, with both strains showing association that was significantly higher than that of L. plantarum No. 14. In a separate experiment, the number of total bacteria and lactobacilli in the gut, as estimated by real-time quantitative PCR, was significantly higher in 14- and 21-day-old mice than in 0- and 7-day-old mice. In addition, the number of total bacteria was higher in 21-day-old mice than in 14-day-old mice, and the number of lactobacilli was higher in 7-day-old mice than in 0-day-old mice. These results suggest that gut persistence of administered bacteria in infant mice is species- or strain-specific and is affected by the development of indigenous microbiota. In addition, gut persistence of administered bacteria may not always depend on the tissue association capacity.
A surface protein of Lactobacillus reuteri, mucus adhesion-promoting protein (MapA), is considered to be an adhesion factor. MapA is expressed in L. reuteri strains and adheres to piglet gastric mucus, collagen type I, and human intestinal epithelial cells such as Caco-2. The aim of this study was to identify molecules that mediate the attachment of MapA from L. reuteri to the intestinal epithelial cell surface by investigating the adhesion of MapA to receptor-like molecules on Caco-2 cells. MapA-binding receptor-like molecules were detected in Caco-2 cell lysates by 2D-PAGE. Two proteins, annexin A13 (ANXA13) and paralemmin (PALM), were identified by MALDI TOF-MS. The results of a pull-down assay showed that MapA bound directly to ANXA13 and PALM. Fluorescence microscopy studies confirmed that MapA binding to ANXA13 and PALM was colocalized on the Caco-2 cell membrane. To evaluate whether ANXA13 and PALM are important for MapA adhesion, ANXA13 and PALM knockdown cell lines were established. The adhesion of MapA to the abovementioned cell lines was reduced compared with that to wild-type Caco-2 cells. These knockdown experiments established the importance of these receptor-like molecules in MapA adhesion.
We examined whether feeding high hydrogen generating resistant starch could suppress subacute hepatic ischemia-reperfusion injury. Rats were fed a control diet with or without 20% high amylose cornstarch (HAS) supplementation for 14 days. On day 12, rats were subject to ischemia-reperfusion treatment. Portal hydrogen concentration was higher in the HAS group compared with the control group. Increased plasma alanine and aspartate aminotransferase activities due to ischemia-reperfusion treatment tended to decrease, and a significant reduction was observed by HAS feeding when compared with the control group. In conclusion, HAS, which enhances hydrogen generation in the hindgut, alleviated subacute hepatic ischemia-reperfusion injury.
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