Helicobacter pylori infection is an important risk factor for gastric diseases. Some probiotics are useful for suppressing H. pylori infection. Bifidobacterium bifidum YIT 4007 can improve the experimental gastric injury in rats and the disease stages on the gastric mucosa in peptic ulcer patients. We evaluated the fermented milk using a clone (BF-1) having the stronger ability to survive in the product than this parent strain to clarify the in vitro suppressive effect of BF-1 on H. pylori and the in vivo efficacy of BF-1 fermented milk on H. pylori and gastric health. In the mixed culture assay of BF-1 and H. pylori, the number of pathogens was decreased such that it was not detected after 48 h in the Brucella broth with a decrease in pH values. In the cell culture experiment with human gastric cells, the H. pylori infection-induced IL-8 secretion was suppressed by the preincubation of BF-1. In a human study of 12-wk ingestion (BF-1 group, n = 40; placebo group, n = 39) with a randomized double-blind placebo-control design, the H. pylori urease activity and gastric situation were evaluated using a urea breath test (UBT) and the serum pepsinogen (PG) levels as biomarkers for inflammation or atrophy, respectively. In the H. pylori-positive subjects, the difference (DeltaUBT) of the UBT value from the baseline value in the BF-1 group (n = 34) was lower than that in the placebo group (n = 35) at 8 wk. The baseline UBT values showed a negative correlation with DeltaUBT values at 8 and 12 wk in the BF-1 group but not in the placebo. In the PG-positive subjects classified by the PG test method, the BF-1 group was lower in DeltaUBT values than the placebo group at 8 and 12 wk. In the active gastritis class by PG levels, the BF-1 group was lower in their DeltaUBT values than the placebo at 8 and 12 wk. The PG I levels in the BF-1 group were lower than the placebo at 12 wk. The PG II levels in the BF-1 group did not change during the ingestion period, but the placebo was increased. The PG I/II ratios slightly decreased from baseline at 12 and 20 wk in the BF-1 and placebo groups. These patterns were also observed in the H. pylori-positive subjects. The improving rates of upper gastrointestinal symptomatic subjects and total symptom numbers in the BF-1 group were higher than those in the placebo. These results indicate that BF-1 fermented milk may affect H. pylori infection or its activity, gastric mucosal situation, and the emergence of upper gastrointestinal symptoms.

The whole nucleotide sequence of pHY300PLK (Ishiwa and Shibahara 1985a) has been determined, pHY300PLK consists of 4870 by and contains an RNA primer for on-177 and three open reading frames corresponding to TcR, ApR and Rep-al. Twenty-three unique restriction endonuclease recognition sites were found. We have confirmed that ORF al of pHY300PLK is the plasmid replication gene. A rescue phenomenon has been found with respect to multiple infection by pHY300.2PLK (rep-) and pUB110. A series of experiments indicated that the oligomer form, pHY300.2PLK, was rescued by the monomeric form, pUB110. Additionally, some useful information for using pHY300PLK as a shuttle vector in molecular cloning studies is presented.

Homeostasis in the stomach environment is maintained by the balance of protective factors such as gastric mucus and aggressive factors such as gastric acid, stress, alcohol, and drugs. An overload of aggressive factors that upsets this balance can induce gastric injury. Fermented milk that contains Bifidobacterium bifidum BF-1 (BF-1), a probiotic strain, and Streptococcus thermophilus YIT 2021 (ST) is known to improve Helicobacter pylori-associated gastritis in humans. Here, we investigated the gastroprotective potential of BF-1 in a rat model of acid-ethanol-induced acute gastric injury to fully elucidate its potential compared with ST. Living BF-1, ST, or vehicle was orally administrated to rats, and acid-ethanol gastric injury was induced 2h later. The gastric injury rate was determined and shown to be significantly lower in the BF-1 group than in the vehicle group, which showed a similar level to the ST group. The production of gastric mucin and the expression of several target genes associated with protection and inflammation were examined before and after induction of gastric injury. Interestingly, mucin 5ac (muc5ac) gene expression in gastric corpus samples and gastric mucin production in stomach samples from the BF-1 group, but not the ST group, were significantly higher than those in the respective samples from the vehicle group. These findings indicate that BF-1 has the potential to provide gastroprotection, alleviating acute gastric injury by enhancing the production of gastric mucin in a rat model.

Oxidative stress in the colon is associated with the incidence of colon cancer. In situ, the suppression of oxidative stress in the colon would be an effective form of prevention of the cancer. In this study we investigated the transit of the radical scavenging activity of milk products through the hamster intestinal tract. Two types of skim milk products were prepared by Maillard reaction and then lactic acid fermentation. Heat treatment enhanced the radical scavenging activity for 2,2-diphenyl-1-picrylhydrazyl radical of skim milk. The activity was further increased by fermentation with Lactobacillus casei strain Shirota. Normal hamsters were fed these milk products for 14 d. For potential radical scavenging activity per unit dry weight of feces and cecal content, the groups ranked in the order of fermented product-fed hamsters > heated product-fed hamsters > control hamsters, reflecting the order of the potential of the corresponding diets. Approximately 12% of the activity of the heated and the fermented product diets passed through the gastrointestinal tract. These results suggest that some of the radical scavenging activity generated by food processing reached the colon in nonabsorbable products.

Helicobacter pylori infection alters gene expression in host cells. Specifically, inflammatory chemokines such as IL-8 are upregulated in the gastric mucosa during H. pylori infection. Although the mechanism by which H. pylori causes inflammation of the gastric mucosa is not yet understood, many studies have suggested that nuclear factor kappa B (NF-κB) plays a key regulatory role in host cells. We have shown that preincubation with Bifidobacterium bifidum strain BF-1, a probiotic strain known to improve H. pylori-associated gastritis, suppresses induction of IL-8 by the pathogen. To investigate how how BF-1 affects gene expression in H. pylori-infected cells, we performed microarray analysis to assess gene expression in epithelial cells, which had been preincubated with BF-1 and infected with H. pylori. We found that preincubation with BF-1 suppresses the expression of H. pylori-induced genes in human cells and that most of the affected genes are related to the NF-κB signaling pathways. These results suggest that BF-1 can affect the regulatory mechanism of the NF-κB signaling pathways.