Vaccination prevents<i>Helicobacter pylori</i>-induced alterations of the gastric flora in mice

Aebischer, Toni; Fischer, André; Walduck, Anna; Schlötelburg, Cord; Lindig, Mirko; Schreiber, S.; Meyer, Thomas; Bereswill, Stefan; Göbel, Ulf B.

doi:10.1111/rp10.1016-j.femsim.2004.05.008

Cited by 63 publications

(54 citation statements)

References 27 publications

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“…In fact, some of the included studies did not find significant differences using cloning (14) and culture-based approaches (19,21), whereas other studies report significant changes in gastric microbiota according to H. pylori status based on DNA microarrays (17) or 454-pyrosequencing (16), which allow the study of a wider range of bacteria, thus providing a more complete view of the picture. Animal studies have also yielded contradicting findings, as H. pylori infection altered significantly the constitution of gastric microbiota in a BALB/c mice model (27) and in Mongolian gerbils (28), but it does not significantly alter the murine gastric microbiota (29).…”

Section: Discussionmentioning

confidence: 89%

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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Section: Discussionmentioning

confidence: 89%

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

et al. 2016

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“…This potential colonization by bacteria in the stomach may help drive the continuing chronic inflammation seen in both our mouse model and in the human disease. One recent study has shown that the gastric microbiota of BALB/c mice infected with H. pylori does change from being predominately lactobacilli to including Clostridia, Bacteroides/Prevotella spp., Eubacterium spp., Ruminococcus spp., Streptococci, and E. coli (Aebischer et al 2006). The importance of this increased microbiological diversity on the progression to gastric adenocarcinoma has not been evaluated.…”

Section: Discussionmentioning

confidence: 99%

Gastric Mucus Alterations Associated With MurineHelicobacterInfection

Schmitz

Durham

et al. 2009

J Histochem Cytochem.

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The C57BL/6 mouse has been shown to develop gastric adenocarcinoma after Helicobacter felis infection. This model was used to determine whether mucin and trefoil factor (TFF) expression after infection was altered in a similar fashion to the changes seen in the protective gastric mucus layer of the human stomach after H. pylori infection. Our results indicate that this mouse model mimics many of the changes seen after human H. pylori infection, including increased expression of muc4 and muc5b and loss of muc5ac. These alterations in mucin expression occurred as early as 4 weeks postinfection, before the development of significant mucous metaplasia or gastric dysplasia. The decrease in muc5ac expression occurred only in the body of the stomach and was not secondary to the adaptive immune response to infection, because a similar decrease in expression was seen after infection of B6.Rag-1−/− mice, which lack B and T cells. Intriguingly, the increased expression of Muc4 and Muc5b in infected C57BL/6 mice was not seen in the infected B6.Rag-1−/− mice. Because B6.Rag-1−/− mice do not develop gastric pathology after H. felis infection, these findings point to the potential role of Muc4 and Muc5b in disease progression. This manuscript contains online supplemental material at http://www.jhc.org . Please visit this article online to view these materials. (J Histochem Cytochem 57:457–467, 2009)

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“…Due to the different stomach physiology of the gerbil (28,29) and the previously demonstrated crucial role of core chemotaxis factors for gerbil colonization (7), we reasoned that it might be very relevant to investigate the functions of H. pylori TlpD also in the gerbil. In particular, the pH in the gerbil stomach lumen is considerably lower than that in the mouse stomach lumen (30), close to the pH of 1 to 2 that is reached in the human stomach lumen, so bacterial abilities related to pH changes in the gastric mucosa might lead to a more severely attenuated colonization phenotype in the gerbil than in the mouse (28,29).…”

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confidence: 99%

Role of Energy Sensor TlpD of Helicobacter pylori in Gerbil Colonization and Genome Analyses after Adaptation in the Gerbil

et al. 2013

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cHelicobacter pylori maintains colonization in its human host using a limited set of taxis sensors. TlpD is a proposed energy taxis sensor of H. pylori and dominant under environmental conditions of low bacterial energy yield. We studied the impact of H. pylori TlpD on colonization in vivo using a gerbil infection model which closely mimics the gastric physiology of humans. A gerbil-adapted H. pylori strain, HP87 P7, showed energy-dependent behavior, while its isogenic tlpD mutant lost it. A TlpD-complemented strain regained the wild-type phenotype. Infection of gerbils with the complemented strain demonstrated that TlpD is important for persistent infection in the antrum and corpus and suggested a role of TlpD in horizontal navigation and persistent corpus colonization. As a part of the full characterization of the model and to gain insight into the genetic basis of H. pylori adaptation to the gerbil, we determined the complete genome sequences of the gerbil-adapted strain HP87 P7, two HP87 P7 tlpD mutants before and after gerbil passage, and the original human isolate, HP87. The integrity of the genome, including that of a functional cag pathogenicity island, was maintained after gerbil adaptation. Genetic and phenotypic differences between the strains were observed. Major differences between the gerbil-adapted strain and the human isolate emerged, including evidence of recent recombination. Passage of the tlpD mutant through the gerbil selected for gain-of-function variation in a fucosyltransferase gene, futC (HP0093). In conclusion, a gerbil-adapted H. pylori strain with a stable genome has helped to establish that TlpD has important functions for persistent colonization in the stomach. Helicobacter pylori chronically colonizes the gastric mucus layer of humans and induces chronic gastritis and, in severe cases, mucosa-associated lymphoid tissue lymphoma or adenocarcinoma of the stomach (1). Motility and chemotaxis are crucial features during the initiation and the persistence of H. pylori colonization, as demonstrated in vivo in mice and Mongolian gerbils (2-8). Chemotaxis allows bacteria to sense environmental stimuli and to navigate toward optimal living conditions. This is particularly important for H. pylori under the harsh conditions of the human stomach. It has been shown that H. pylori loses its motility within minutes in vivo under conditions of low pH and high pepsin activity (9). A proper orientation determined by a combination of stomach conditions/physiology and optimal bacterial tactic abilities is also required for H. pylori to reach its destination during the initial colonization process (10). Indeed, the majority of H. pylori cells detected in vivo in the Mongolian gerbil stomach were located in intimate proximity to the epithelial cells and were guided there by a vertical pH gradient in the stomach mucus (11).In H. pylori, a complete set of chemotaxis genes has been identified, including the established core genes and genes coding for four transducer-like proteins (Tlps), TlpA, TlpB, TlpC, ...

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Vaccination preventsHelicobacter pylori-induced alterations of the gastric flora in mice

Cited by 63 publications

References 27 publications

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

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

Gastric Mucus Alterations Associated With MurineHelicobacterInfection

Role of Energy Sensor TlpD of Helicobacter pylori in Gerbil Colonization and Genome Analyses after Adaptation in the Gerbil

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