Upper Gastrointestinal Tract Probiotics as a Tool for the Management of Helicobacter pylori
Oscar Brunser, MD, Sylvia Cruchet, MD and Martin Gotteland, PhD Laboratory of Microbiology and Probiotics, Institute of Nutrition and Food Technology, University of Chile
Abstract
Helicobacter pylori is a lifelong component of the gastric microbiota of 50–60% of the world population and the main cause of gastritis, peptic ulcers, and gastric cancer and its eradication is associated with improvement of gastric mucosal inflammation. The colonization and virulence factors of H. pylori: motility, environmental sensing, resistance to gastric hydrochloric acid (HCl), and the release of cytotoxins explain some of its detrimental effects. As the majority of human carriers are asymptomatic it is not reasonable to attempt eradication with antibiotics. Instead, probiotics represent an alternative as they resist gastric pH, and inhibit the growth of H. pylori and its adhesion to the gastric epithelial cells; in addition, the supernatants of their cultures inhibit the multiplication of the pathogen in vitro. Additionally, probiotics exert antioxidant and anti-inflammatory effects in experimental animals and improve the gastric mucosa barrier function in humans. In clinical studies some probiotic strains eradicate H. pylori by themselves in 12–14% of colonized children and adults. These probiotics also decrease the numbers of colonizing organisms and, concomitantly, the severity of mucosal inflammation. When administered with antibiotics, probiotics decrease their secondary effects; consequently, probiotics are useful in the management of H. pylori colonization and its effects.
Keywords Helicobacter pylori, colonization, gastritis, gastric cancer, triple therapy, probiotics, Lactobacillus, Bifidobacterium, Saccharomyces boulardii
Disclosure: The authors have no conflicts of interest to declare. Received: April 7, 2010 Accepted: October 19, 2010 Citation: US Gastroenterology & Hepatology Review, 2010;6:22–6 Correspondence: Oscar Brunser, MD, Gastroenterology Unit, INTA, Avda, El Líbano 5524 – Macul, Casilla 138-11, Santiago, Chile. E:
obrunser@inta.cl/
Brunser@entelchile.net
Helicobacter pylori is a lifelong component of the gastric microbiota in about 50–60% of the world’s population. It colonises considerably earlier, and at higher rates, in the less developed countries, where it may affect up to 90% of the adult population. In comparison, only 9–30% of adults are infected in developed countries, and this infection generally occurs much later in life.1
When the pathogen is eradicated, ulcer healing occurs and the eventual progression of chronic gastritis to atrophic gastritis is interrupted, resulting in a lower risk for gastric adenocarcinoma or mucosa-associated lymphoid tissue (MALT) lymphoma.1
H. pylori is the main cause of gastritis, peptic ulcers, and gastric carcinoma and lymphoma. It is estimated that 80% of all peptic ulcers are associated with the presence of H. pylori, with most of the remaining cases due to non-steroidal anti-inflammatory drugs (NSAIDS).1
The National
Institutes of Health (NIH) Consensus Development Panel on Helicobacter pylori in Peptic Ulcer Disease of 1994 considered H. pylori as a type I carcinogen.
H. pylori is a spiral-shaped Gram-negative organism that is associated with the mucus layer overlying the surface epithelium, but does not colonize the deeper parts of the gastric glands.2
effects of hydrochloric acid (HCl). The resistance to HCl is related to the presence of more than 300 acid-regulated enzymes—including urease, which hydrolyses gastric urea—that produce carbon dioxide and ammonia, raising the pH in the vicinity of the bacteria and allowing for its survival in the gastric lumen. Urease constitutes the basis for the detection of H. pylori in gastric mucosal biopsies along with the 13C urea breath test (UBT), which allows for its non-invasive detection.3
Adherence of H. pylori to gastric epithelial cells activates bacterial genes, some encoding virulence factors. As a reaction to this adherence, the epithelial cells form pedestals in the area of contact and some bacteria may become intracellular. H. pylori survives in vitro in the cytoplasm of neutrophils and monocytes, but the significance of this capability in vivo is not known.4
H. pylori induces intense immune and
inflammatory reactions associated with the infiltration of neutrophils, lymphocytes, and monocytes to the gastric mucosa, while stimulating systemic antibody and cell-mediated responses that are ineffective in clearing the infection.3
Its colonization factors include motility, environmental sensing, and the capacity to resist the 22
The persistence of H. pylori throughout the life of the host, the relatively small proportion of colonized individuals who develop peptic ulcers— about 15%—and the even smaller proportion who develop malignancies are the result of interaction between the virulence factors of the
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