Probiotics as a Tool for the Management of Helicobacter pylori
micro-organism, the defensive mechanisms and genetic background of the host, and external factors such as quality of diet and smoking.5
The distribution of these virulence markers in the population varies from country to country. Strains of H. pylori associated more frequently with ulceration or adenocarcinoma are cytotoxin-associated gene A + (cagA+) whereas cagA- strains are seldom associated with these diseases. The vacuolating cytotoxin gene vacA is present in all strains of H. pylori. Some forms of H. pylori are practically non-toxic; others have been associated with a high incidence of adenocarcinoma.7 Other virulence factors detected in H. pylori include outer inflammatory proteins, adhesins, blood group antigen-binding adhesin-A, and a number of different methylases.8
The virulence factors detected in H. pylori include the cytotoxin- associated gene pathogenicity island (PAI), which includes some 30 genes.6
Interestingly, H. pylori may also modify
leptin and ghrelin production and, by interfering with the mechanisms of hunger and satiety, it may influence bodyweight and the tendency to obesity.9,10
Cag+ H. pylori are associated with less severe Barrett’s esophagus and a lower incidence of esophageal cancer. Infection with H. pylori has also been associated with extra-digestive diseases, cardiovascular and cerebrovascular diseases, liver and skin diseases, and thrombocytopenic purpura. Further research is required to clarify these aspects.13,14
H. pylori may protect against the consequences of Barrett’s esophagus and esophageal adenocarcinoma and gastroesophageal reflux disease (GERD).11,12
Therapeutic and Dietary Management of Helicobacter pylori Colonization Symptomatic H. pylori infection is classically treated with an inhibitor of the proton pump and two antibiotics, generally amoxicillin and clarythromycin, for seven to 14 days. If antibiotic resistance is verified or suspected, the antibiotics may be substituted with metronidazole or azythromycin. The results of this treatment are variable, with a rate of success between 60 and 90%.15
The treatment causes a number of
secondary effects such as a metallic taste and tingling of the mouth, oral candidiasis, non-specific diarrhea, vomiting, abdominal pain, and allergic reactions. A number of patients interrupt their treatment before completion because of these secondary effects, and for this reason alternatives to the antibiotic treatment or other forms of alleviating secondary effects have been sought. Recurrence after treatment depends on the prevalence of H. pylori colonisation in the population.16
Most individuals colonized by H. pylori, including children, are asymptomatic and cannot be treated with antibiotics, independent of their risk for developing gastric diseases in the future. This risk increases when the time elapsed from the onset of the colonization grows longer. Antibiotic treatment does not eradicate H. pylori from a significant proportion of patients treated. This may be due to antibiotic resistance and the fact that compliance with treatment is unsatisfactory because of the adverse effects. Proper application of the treatment is also limited by its high cost, in particular for families from the lower socioeconomic stratum in whom H. pylori prevalence is higher. In addition, children tend to relapse more frequently and rapidly than adults. It is important to develop low-cost, large-scale alternative
US GASTROENTEROLOGY & HEPATOLOGY REVIEW
solutions applicable to at-risk populations to prevent or decrease H. pylori colonization and its consequences. This article summarises the studies using probiotics as possible protective agents to control H. pylori colonization and decrease gastric inflammation.17
Probiotics are generally recognized as safe micro-organisms. They are mostly lactic acid bacteria such as lactobacilli and bifidobacteria, which are present in high concentrations in some foods. Some yeasts, such as Saccharomyces boulardii, are also considered as probiotics. Probiotic micro-organisms survive during their transit along the gastrointestinal tract where they modulate the gut microbiota and exert health- promoting activities beneficial for the host.18
Among these activities are
the inhibition of pathogens, the modulation of immune responses, the stabilization of the gastrointestinal barrier function, the decrease of pro-carcinogenic enzymatic activities, and the production of enzymatic activities of nutritional interest such as β-galactosidase.
Inhibition of Helicobacter pylori by Probiotics Although a great number of studies have shown that some strains of Lactobacillus spp. and Bifidobacterium spp. can survive in the human stomach,19
it was not clear until recently whether these strains remained metabolically active in this environment. Denou et al. recently explored this point with Lactobacillus johnsonii NCC533, a well- described probiotic strain.20
They observed that the number of genes
expressed by this micro-organism in the stomach was higher than in other gut segments in mice, indicating that it probably remains metabolically active in the stomach. This suggests that this probiotic strain may compete with H. pylori in the gastric ecosystem producing bactericidal substances that interfere with this pathogen.
Various studies support this hypothesis, showing that probiotics may inhibit H. pylori growth owing to the production of short-chain fatty acids (SCFAs) and/or bacteriocins. These studies have been carried out mostly in vitro, with lactic acid as the main SCFA displaying this effect, although formic acid may also be implicated.21–23
The antimicrobial activities of
SCFAs could be due to a direct effect on the pathogen, but also to the inhibition the urease activity, as observed with L. casei Shirota.24
High
lactic acid-producer strains of Lactobacillus were shown to decrease H. pylori density in the stomach of mice, but bacteriocins could be implicated. These are small, heat-resistant, dialyzable peptides with antimicrobial activities that are synthesized by several bacterial genera, including lactic acid bacteria. The release of bacteriocins active against H. pylori has been studied chiefly in Lactobacillus, but probiotic bifidobacteria may also produce them.25
Lacticins produced by strains of
L. lactis are highly potent against H. pylori, with minimum inhibitory concentrations from 0.097–0.390mg/l to 12.5–25mg/l.26
do not survive well in the human digestive tract. The supernatant of a culture of L. johnsonii NCC533 was shown to inhibit both the urease activity and growth of H. pylori free or adherent to epithelial cells.27
activity was heat-resistant and dialyzable and was not affected by 10mM urea, and, therefore, was compatible with a bacteriocin, probably
lactacin-F. Additionally, this probiotic releases H2O2 at concentrations effective against Salmonella, and perhaps active against H. pylori.28
The
administration of an L. johnsonii NCC533 culture supernatant to colonized patients significantly decreased the values of 13C UBT and decreased the severity of the gastric inflammation.27
23 Lactococcus spp. This
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