Regarding the use of Lactobacillus gasseri and other Lactobacillus species for the eradication of Helicobacter pylori bacterial infection. I present some pertinent data for your review.
Helicobacter pylori is a common gastric pathogen with infection resulting in acute and chronic mucosal damage and the possible clinical manifestation of peptic ulcers, gastritis, and gastric cancer due to active infections of long duration. Current treatments include the administration of antibiotics, with or without synergistic nutraceutical support. Treatment of Helicobacter pylori often results in the alleviation of symptoms, but not necessarily the eradication of the bacteria in the host. Consequently, remission can occur and the subsequent infection of Helicobacter pylori can cause antibiotic resistance, upregulation of H. pylori virulence factors, and/or increased biofilm production, of the infectious strain.
There are many synergistic nutraceuticals that help support H. pylori eradication. The focus here will be on Lactobacillus gasseri OLL2716. L gasseri OLL2716. demonstrated In vitro experiments demonstrated that Lactobacillus gasseri inhibited the growth of H. pylori and suppressed H. pylori-associated IL-8 production. Such effects were noted in Clarithromycin (CAM)-resistant and CAM-susceptible H. pylori. Similarly, in an in vivo model of H. pylori infection, H. pylori colonization was significantly decreased by Lactobacillus gasseri. Therefore, L. gasseri was found to act as a probiotic in CAM-resistant Helicobacter pylori infection. (Ushiyama et al., 2003).
The ability of Lactobacillus gasseri OLL2716 to inhibit H. pylori infection was also observed in human clinical trials. A trial with 31 participants infected with H. pylori was fed yogurt containing Lactobacillus gasseri OLL2716 at a level of 107 CFU g−1 daily for 16 weeks, and the urea breath test was performed as a measure of infection. The probiotic yogurt decreased markers for Helicobacter pylori infection 2 weeks after consumption, but not during the treatment. The probiotic yogurt treatment group exhibited decreased H. pylori in antral biopsies as well as the infection marker of serum pepsinogen levels (Sakamoto et al., 2001). Another study evaluated the efficacy of Lactobacillus gasseri in both prevention and treatment of Helicobacter pylori infection in children (Boonyaritichaikij et al., 2009). Lactobacillus gasseri OLL2716 was administered to 82 asymptomatic Helicobacter pylori-infected children for 1 year, who were subsequently assayed for Helicobacter pylori stool antigen to monitor infection. In the treatment group, 42% of the participants had remission 6 months after cessation of treatment, but 24 of the participants were free from infection after 1 year. The consumption of L. gasseri as a preventative measure was not associated with a decrease in the incidence of H. pylori infection. Data from in vitro assays and animal models suggest a potential role for the mitigation and treatment of H. pylori infection by administration of Lactobacillus gasseri OLL2716, but more clinical trials will be needed to substantiate its clinical relevance.
Interestingly, gnotobiotic mouse* (*refers to mice in which every microorganism present is defined. Germ-free mice are one class of gnotobiotic animals) in vivo studies have further indicated the potential of other lactobacilli species to prevent infection entirely when colonized with lactobacilli salivarius (Kabir et al., 1997; Aiba et al., 1998). IL-8 has been implicated in playing a major role in the development of mucosal inflammation and injury in H. pylori infections as it is a chemotactic factor* for neutrophils. Chronic expression of IL-8 due to recurrent H. pylori infection may exacerbate mucosal inflammation and tissue damage (Crabtree & Lindley, 1994). In this regard, co-incubation of Lactobacillus gasseri OLL2716 with an MK45 cell line infected with H. pylori inhibited the expression of IL-8 when compared with the control (Ushiyama et al., 2003). Further investigation of the ability of L. gasseri OLL2716 to inhibit IL-8 yielded similar results but indicated that the probiotic strain neither inhibited the adhesion of H. pylori to infected cells nor interfered with TNF-α-induced IL-8 expression (Tamura et al., 2006). This suggests that the decrease in H. pylori-induced IL-8 expression was mediated by a mechanism independent of the adhesion of the pathogen. The study also reported that the decrease in IL-8 secretion observed in the cell culture line occurred similarly in humans infected with Helicobacter pylori.
Based on the above findings the addition of synergistic compounds that may inhibit H. pylori from adhering to the gastric epithelial cells is warranted and suggested. Fucoidan is one such compound. Fucoidins are complex sulfated polysaccharides derived from edible marine algae, like bladderwrack. fucoidans inhibit H. pylori’s attachment to gastric epithelial cells in vitro (Tey et al., 2015). Specific strains of Lactobacillus acidophilus are known to inhibit intestinal cell adhesion and invasion by enterovirulent bacteria. As Lactobacillus. acidophilus can survive transiently in the human stomach, it may downregulate Helicobacter pylori infection. L. acidophilus (johnsonii) La1 culture supernatant shown to be effective in vitro has a partial, acid-independent long-term suppressive effect on H. pylori in humans (Michetti et al., 1999).
*Chemotaxis (from chemo- + taxis) is the movement of an organism in response to a chemical stimulus. Somatic cells, bacteria, and other single-cell or multicellular organisms direct their movements according to certain chemicals in their environment.
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- Helicobacter pylori Facts and More Facts…
- Blog post – H. pylori-free, in just 34 days, without antibiotics.
- H. pylori Treatment Testimonial – 03/2018
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- Dr. Ettinger’s Biofilm Protocol for Lyme and Gut Pathogens
- Quorum Sensing and Biofilm
- Can H. pylori actually be good for us? An Endangered Species in the Stomach, by Martin J. Blaser
- Probiotics May Represent a Novel Approach to The Management of H. pylori Infection.
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- Ulcer-Causing Helicobacter Pylori Survives In Our Acidic Gut By Turning It Neutral
- Antibiotics Have Turned Our Bodies From Gardens Into Battlefields – an interview with microbiologist, Dr. Martin Blasser
- Helicobacter pylori and cardiovascular complications: a mechanism-based review on the role of Helicobacter pylori in cardiovascular diseases
- The bacterial virulence factor CagA induces microbial dysbiosis that contributes to excessive epithelial cell proliferation in the Drosophila gut.