Factors that mediate colonization of the human stomach byHelicobacter pylori

Dunne, Ciara; Dolan, Brendan; Clyne, Marguerite

doi:10.3748/wjg.v20.i19.5610

Cited by 94 publications

(80 citation statements)

References 147 publications

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“…H. pylori cause chronic gastritis and when left untreated can eventually lead to the development of gastroduodenal ulcers and gastric cancer in a subset of infected individuals (5). Although the majority of Helicobacter bacteria remain in the mucus layer lining the gastric epithelium (6)(7)(8), it is widely accepted that the bacteria in contact with epithelial cells cause disease.…”

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confidence: 99%

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Lactobacilli Reduce Helicobacter pylori Attachment to Host Gastric Epithelial Cells by Inhibiting Adhesion Gene Expression

et al. 2016

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The human gastrointestinal tract, including the harsh environment of the stomach, harbors a large variety of bacteria, of which Lactobacillus species are prominent members. The molecular mechanisms by which species of lactobacilli interfere with pathogen colonization are not fully characterized. In this study, we aimed to study the effect of lactobacillus strains upon the initial attachment of Helicobacter pylori to host cells. Here we report a novel mechanism by which lactobacilli inhibit adherence of the gastric pathogen H. pylori. In a screen with Lactobacillus isolates, we found that only a few could reduce adherence of H. pylori to gastric epithelial cells. Decreased attachment was not due to competition for space or to lactobacillus-mediated killing of the pathogen. Instead, we show that lactobacilli act on H. pylori directly by an effector molecule that is released into the medium. This effector molecule acts on H. pylori by inhibiting expression of the adhesin-encoding gene sabA. Finally, we verified that inhibitory lactobacilli reduced H. pylori colonization in an in vivo model. In conclusion, certain Lactobacillus strains affect pathogen adherence by inhibiting sabA expression and thereby reducing H. pylori binding capacity.

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confidence: 99%

“…Helicobacter pylori is a Gram-negative, helix-shaped, microaerophilic, human-specific bacterium that colonizes the stomach of more than half of the world's population (5). H. pylori cause chronic gastritis and when left untreated can eventually lead to the development of gastroduodenal ulcers and gastric cancer in a subset of infected individuals (5).…”

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Lactobacilli Reduce Helicobacter pylori Attachment to Host Gastric Epithelial Cells by Inhibiting Adhesion Gene Expression

et al. 2016

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“…Helicobacter pylori (H. pylori) is a spiral-shaped, microaerophilic, gram-negative bacterium that establishes persistent infection in the stomach and causes gastric inflammation, which contributes to the progression of various gastric diseases such as chronic gastritis, gastric ulcers, and gastric cancer (4,24,26,27). Many investigators have reported the relevance of cytokine production to H. pylori infection (23,34).…”

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Helicobacter pylori induces IL-1β protein through the inflammasome activation in differentiated macrophagic cells

et al. 2016

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More than 50% of people in the world are infected with Helicobacter pylori (H. pylori), which induces various gastric diseases. Especially, epidemiological studies have shown that H. pylori infection is a major risk factor for gastric cancer. It has been reported that the levels of interleukin (IL)-1β are upregulated in gastric tissues of patients with H. pylori infection. In this study, we investigated the induction mechanism of IL-1β during H. pylori infection. We found that IL-1β mRNA and protein were induced in phorbol-12-myristate-13-acetate (PMA)-differentiated THP-1 cells after H. pylori infection. This IL-1β production was inhibited by a caspase-1 inhibitor and a ROS inhibitor. Furthermore, K + efflux and Ca 2+ signaling were also involved in this process. These data suggest that NOD-like receptor (NLR) family, pyrin domain containing 3 (NLRP3) and its complex, known as NLRP3 inflammasome, are involved in IL-1β production during H. pylori infection because it is reported that NLRP3 inflammasome is activated by ROS, K + efflux and/or Ca 2+ signaling. These findings may provide therapeutic strategy for the control of gastric cancer in H. pylori-infected patients.

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“…pylori colonizes in the stomach of more than 50% the world's population. Majority of these bacteria occur in the mucus layer of the stomach and may act as a reservoir of infection for the underlying gastric epithelium (Dunne et al, 2014). Moreover, it is widely accepted that the bacteria in contact with epithelial cells initiate disease (Klerk et al, 2016).…”

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confidence: 99%

Helicobacter pylori in ice cream and its control using mastic gum essential oil

Saad¹,

El‐Zamkan²

2017

J Adv Vet Anim Res

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Objective: This study aimed at assessing the prevalence of Helicobacter spp. in ice cream sold at Qena city (Egypt) with special reference to H. pylori, and to study the antimicrobial effect of mastic gum essential oil on H. pylori. Materials and methods: A total of 60 small and large scale ice cream samples (30 each) were investigated for the presence of Helicobacter spp. Then, the essential oil of mastic gum was added to lab prepared ice cream inoculated with H. pylori isolate in a count of Log6 using 2 concentrations of 0.8 and 1.6% and one group was kept as a control group. Each group was subdivided into 2 sub-groups; one was kept at -5°C and another one was kept at -20°C. Results: Helicobacter spp. could be isolated from 11.7%, while, H. pylori could be found in 3.3% of the total examined ice cream samples. Regarding the antiHelicobacter pylori effect of mastic gum essential oil added to lab prepared ice cream, in samples kept at -5°C it was found that after hardening the count fall into Log5 in both control and 0.8% groups and log4 in 1.6% essential mastic oil concentration. Reduction in H. pylori at the first week and third day of storage reached 100% where H. pylori couldn't be counted or isolated from both 0.8 and 1.6% concentrations, respectively. While in ice cream samples stored at -20°C, the reduction in H. pylori load was rapid at first, it was log4 and log3 in groups of 0.8% and 1.6% concentrations, respectively versus log5 in control samples. At the third day H. pylori was not able to be counted or isolated at third day of storage for both concentrations. Conclusion: All isolates recovered from small scale ice cream samples reflexing the hygienic conditions under which samples were produced. Mastic gum essential oil exhibited a powerful anti-H. pylori effect recommending its addition to food matrix for therapeutic purposes or as a functional food.

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Factors that mediate colonization of the human stomach byHelicobacter pylori

Cited by 94 publications

References 147 publications

Lactobacilli Reduce Helicobacter pylori Attachment to Host Gastric Epithelial Cells by Inhibiting Adhesion Gene Expression

Lactobacilli Reduce Helicobacter pylori Attachment to Host Gastric Epithelial Cells by Inhibiting Adhesion Gene Expression

<i><b>Helicobacter pylori</b></i><b> induces IL-1β protein through the inflammasome activation in differentiated macrophagic </b><b>cells </b>

Helicobacter pylori in ice cream and its control using mastic gum essential oil

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