Reply to M Gotteland et al

Department of Internal Medicine
Kaohsiung Medical University Hospital
Kaohsiung
Taiwan
E-mail: gi{at}kmu.edu.tw

Dear Sir:

Probiotic strains are assumed to exert their effect on the microecology and metabolism of the colon by passing through the upper gastrointestinal tract. The metabolic capability of colonic microbes on ingested foods could affect the upper gastrointestinal tract physiology, such as lower esophageal sphincter or proximal gastric tone through the neurohumoral mechanism, or they could produce abdominal symptoms by aberrant fermentation. The alteration of microbial flora of the colon, either by antibiotic or probiotics therapy, was associated with symptom improvement and reduction in gas production in a subset of patients with functional bowel disease.

A growing body of recent evidence suggests that regular intake of probiotics suppresses Helicobater pylori infection in humans (1, 2). However, it remains unclear whether these probiotic strains act exclusively on the gastric mucosa, much in the same way as they act on the colonic mucosa—ie, by adhering to the mucosal surface and inhibiting the attachment of other pathogenic bacteria and by secreting a factor or factors that enhance the barrier integrity and the immunomodulatory function of cells of the local immune system (3)—or whether, alternatively, they act by potentially altering colonic hydrogen production to reduce the energy source for H. pylori survival in the stomach (4) and thus have a beneficial effect on H. pylori–associated gastritis.

Marteau et al (5) reported that the area under the curve for breath-hydrogen production was lowest after subjects consumed a fermented dairy product containing Bifidobacterium bifidum, Lactobacillus acidophilus, and mesophilic bacteria. Bouhnik et al (6) observed a significant reduction in breath hydrogen and an increase in fecal bifidobacteria in 8 healthy subjects consuming transgalactooligosaccharides. In a study by Pantoflickova et al (1), there was no significant change in the fecal counts of Bifidobacteria, Enterobacteria, or Clostridium difficile after regular intake of fermented milk containing Lactobacillus johnsonii. In contrast, in a study of 34 subjects consuming the same yogurt as in our study (fermented milk containing galactooligosaccharide, Lactobacillus bulgaricus, L. acidophilus, and B. bifidum), an arbitrarily primed polymerase chain reaction method detected the proliferation of ingested B. bifidum in the stool (7). An earlier report showed elevated amounts of breath hydrogen and fecal bifidobacteria in 12 healthy volunteers consuming a yogurt drink containing Bifidobacteria longum and lactulose. The authors attributed the effects to the addition of laculose and the consumption of yogurt per se, respectively (8). To test the hypothesis that bifidobacteria consumption will decrease hydrogen production, a double-blind crossover study of 13 healthy subjects ingesting bifidobacteria for 12 d was conducted. No significant changes in either breath hydrogen or fecal bifidobacteria were found (9). Sen et al (10) conducted a study in patients with irritable bowel syndrome that showed the intake of Lactobacilli plantarum 299v and lactulose to significantly reduce breath-hydrogen excretion. These findings suggest that the results of colonic fermentation after the intake of food or probiotics vary and could depend on the substrate added and the status of the study subjects. To examine this possibility, future studies addressing the association between the severity of gastritis and breath-hydrogen concentration are required.

ACKNOWLEDGMENTS

None of the authors had any personal or financial conflicts of interest.

REFERENCES

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