The role of the gastrointestinal microbiome in
            <i>
              <i>Helicobacter pylori</i>
            </i>
            pathogenesis

Sheh, Alexander; Fox, James G.

doi:10.4161/gmic.26205

Cited by 179 publications

(167 citation statements)

References 170 publications

(324 reference statements)

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“…Lactobacillus spp. have also been found in the stomach microbiome (28). Lactobacillus suebicus isolated from fruit mash is able to grow at pH 3.0 and in the presence of 14% ethanol (29).…”

Section: Common Stresses Encountered By Lab In Their Ecological Nichesmentioning

confidence: 99%

Stress Physiology of Lactic Acid Bacteria

Papadimitriou

Alegría

Bron

et al. 2016

Microbiol Mol Biol Rev

539

404

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SUMMARYLactic acid bacteria (LAB) are important starter, commensal, or pathogenic microorganisms. The stress physiology of LAB has been studied in depth for over 2 decades, fueled mostly by the technological implications of LAB robustness in the food industry. Survival of probiotic LAB in the host and the potential relatedness of LAB virulence to their stress resilience have intensified interest in the field. Thus, a wealth of information concerning stress responses exists today for strains as diverse as starter (e.g.,Lactococcus lactis), probiotic (e.g., severalLactobacillusspp.), and pathogenic (e.g.,EnterococcusandStreptococcusspp.) LAB. Here we present the state of the art for LAB stress behavior. We describe the multitude of stresses that LAB are confronted with, and we present the experimental context used to study the stress responses of LAB, focusing on adaptation, habituation, and cross-protection as well as on self-induced multistress resistance in stationary phase, biofilms, and dormancy. We also consider stress responses at the population and single-cell levels. Subsequently, we concentrate on the stress defense mechanisms that have been reported to date, grouping them according to their direct participation in preserving cell energy, defending macromolecules, and protecting the cell envelope. Stress-induced responses of probiotic LAB and commensal/pathogenic LAB are highlighted separately due to the complexity of the peculiar multistress conditions to which these bacteria are subjected in their hosts. Induction of prophages under environmental stresses is then discussed. Finally, we present systems-based strategies to characterize the “stressome” of LAB and to engineer new food-related and probiotic LAB with improved stress tolerance.

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“…Lactobacillus spp. have also been found in the stomach microbiome (28). Lactobacillus suebicus isolated from fruit mash is able to grow at pH 3.0 and in the presence of 14% ethanol (29).…”

Section: Common Stresses Encountered By Lab In Their Ecological Nichesmentioning

confidence: 99%

Stress Physiology of Lactic Acid Bacteria

Papadimitriou

Alegría

Bron

et al. 2016

Microbiol Mol Biol Rev

539

404

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“…It is possible that gastric microbiota constitutes the link between H. pylori and gastric carcinogenesis, when other bacteria colonize the stomach under conditions of decreased acidity (such as chronic atrophic gastritis), creating reactive oxygen and nitrogen species and modulating inflammatory responses (12,13). Therefore, it is important to unravel the significance of specific microbiota to determine which ones are causative of gastric cancer and which are present merely as a consequence in order to develop novel prevention and treatment strategies.…”

Section: Introductionmentioning

confidence: 99%

Gastric microbiota and carcinogenesis: the role of non-Helicobacter pylori bacteria - A systematic review

et al. 2016

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Background and aim:Helicobacter pylori is the strongest risk factor for gastric cancer. However, recent advances in DNA sequencing technology have revealed a complex microbial community in the stomach that could also contribute to the development of gastric cancer. The aim of this study was to present recent scientific evidence regarding the role of non-Helicobacter pylori bacteria in gastric carcinogenesis.Methods: A systematic review of original articles published in PubMed in the last ten years related to gastric microbiota and gastric cancer in humans was performed.Results: Thirteen original articles were included. The constitution of gastric microbiota appears to be significantly affected by gastric cancer and premalignant lesions. In fact, differences in gastric microbiota have been documented, depending on Helicobacter pylori status and gastric conditions, such as non-atrophic gastritis, intestinal metaplasia and cancer. Gastric carcinogenesis can be associated with an increase in many bacteria (such as Lactobacillus coleohominis, Klebsiella pneumoniae or Acinetobacter baumannii) as well as decrease in others (such as Porphyromonas spp, Neisseria spp, Prevotella pallens or Streptococcus sinensis). However, there is no conclusive data that confirms if these changes in microbiota are a cause or consequence of the process of carcinogenesis.Conclusions: Even though there is limited evidence in humans, microbiota differences between normal individuals, premalignant lesions and gastric cancer could suggest a progressive shift in the constitution of gastric microbiota in carcinogenesis, possibly resulting from a complex cross-talk between gastric microbiota and Helicobacter pylori. However, further studies are needed to elucidate the specific role (if any) of different microorganisms.

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“…Conventional wisdom espoused the dogma that pH values < 4 were able to sterilize the stomach, but since the discovery of H. pylori [94] , a complex community of noncultivatable inhabitants have been uncovered in the stomach [95] . The interaction of gastric microbiota with H. pylori likely affects gastric immunobiology and the outcome of infection [95] .…”

Section: Gastric Microbiotamentioning

confidence: 99%

“…The interaction of gastric microbiota with H. pylori likely affects gastric immunobiology and the outcome of infection [95] . Data indicate that the microbial density in the normal stomach is low (10 1 10 3 CFU/g) [94] , and the low bacterial densities within this portion of gastrointestinal tract is attributed to rapid peristalsis, low pH and/or high bile concentration [96] . The parietal cell loss caused by H. pylori infection leads to hypoch lorhydria or even achlorhydria, thereby increase the risk of bacterial overgrowth and detrimental infection [97] .…”

Section: Gastric Microbiotamentioning

confidence: 99%

Role ofHelicobacter pyloriinfection in pathogenesis of gastric carcinoma

Zhang

Fan

Chen

2016

WJGP

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Gastric cancer (GC) is one of the most common carcino ma and the second leading cause of cancerrelated deaths worldwide. Helicobacter pylori (H. pylori ) infection causes a series of precancerous lesions like gastritis, atrophy, intestinal metaplasia and dysplasia, and is the strongest known risk factor for GC, as supported by epidemiological, preclinical and clinical studies. However, the mechanism of H. pylori developing gastric carcinoma has not been well defined. Among infected individuals, approximately 10% develop severe gastric lesions such as peptic ulcer disease, 1%3% progresses to GC.

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The role of the gastrointestinal microbiome in Helicobacter pylori pathogenesis

Cited by 179 publications

References 170 publications

Stress Physiology of Lactic Acid Bacteria

Stress Physiology of Lactic Acid Bacteria

Gastric microbiota and carcinogenesis: the role of non-Helicobacter pylori bacteria - A systematic review

Role ofHelicobacter pyloriinfection in pathogenesis of gastric carcinoma

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