Consumption of exogenous bifidobacteria does not alter fecal bifidobacteria and breath hydrogen excretion in humans.

The hypothesis that consumption of bifidobacteria by humans would increase colonic bifidobacteria and decrease breath hydrogen excretion was examined. A commercially available strain of bifidobacteria was tracked through the gastrointestinal tract. We determined that a 12-d feeding period of 10(10) cells of exogenous bifidobacteria daily was adequate to achieve a stable number of exogenous bifidobacteria in the colon. A 12-d washout period was chosen because the exogenous bifidobacteria could no longer be detected at that time. A double-blind crossover study used both male and female subjects. The order of treatment with skim milk alone or skim milk + bifidobacteria was randomized. Breath hydrogen excretion (micromol/L) and fecal counts of total bifidobacteria [log colony forming units (CFU)/g feces] were not significantly different between males and females and were not affected by consumption of exogenous bifidobacteria. Calculations based on the numbers of exogenous bifidobacteria consumed and the fecal numbers of exogenous bifidobacteria excreted suggested that numbers of the exogenous strain increased within the gastrointestinal tract. These data suggest that it is difficult to permanently alter total colonic bifidobacteria and affect physiologic function (net hydrogen in the colon as reflected by breath hydrogen) by feeding bifidobacteria, although the percentage of the total bifidobacteria represented by the exogenous strain can be affected.

Differentiation of ingested and endogenous bifidobacteria by DNA fingerprinting demonstrates the survival of an unmodified strain in the gastrointestinal tract of humans.

Consumption of bifidobacteria as a dietary adjunct has received considerable attention for its possible role in the maintenance of gastrointestinal health. However, speculation exists about these presumed health benefits because of an inability to assess the fate and mechanism of action of ingested bifidobacteria. Thus, our objective was to examine the fate of ingested bifidobacteria through the gastrointestinal tract. Variations in the highly conserved 16S ribosomal DNA (rDNA) of bifidobacteria from six male subjects (18 to 35 y old) were assessed by restriction fragment length polymorphism (RFLP) analysis. During the 16-d study, 10(10) colony-forming units (CFU) of a commercially available bifidobacteria were delivered to subjects in fluid milk for each of 8 d. During the remaining 8 d, subjects consumed milk without bifidobacteria. Feces were collected at 4-d intervals and plated on selective media. For each subject, 10-15 colonies were randomly selected and used as template for PCR-amplification of 16S rDNA. 16S rDNA was restriction digested and resolved by electrophoresis. The 16S rDNA-RFLP of the ingested bifidobacteria was unique compared with bifidobacteria found in subjects prior to the feeding study. When subjects consumed bifidobacteria, a 16S rDNA-RFLP identical to that of the ingested bifidobacteria was observed in feces. The concentration of the ingested bifidobacteria in feces increased to 67.2 +/- 8.5% (mean +/- SEM) of total bifidobacteria. After feeding stopped, the ingested bifidobacteria diminished and became undetectable. Using this molecular approach to monitor ingested bifidobacteria, we demonstrate the kinetics of passage of this organism through the gastrointestinal tract of healthy humans.