BabA-mediated Adherence Is a Potentiator of the Helicobacter pylori Type IV Secretion System Activity

Ishijima, Nozomi; Suzuki, Masato; Ashida, Hiroshi; Ichikawa, Yukimi; Kanegae, Yumi; Saito, Izumu; Borén, Thomas; Haas, Rainer; Sasakawa, Chihiro; Mimuro, Hitomi

doi:10.1074/jbc.m111.233601

Cited by 165 publications

(142 citation statements)

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“…Some studies suggest that patients infected with H. pylori strains expressing BabA are more likely to develop peptic ulcer disease or gastric cancer (14,15), particularly if the cagPAI is also present. These epidemiological observations have been supported by in vitro and in vivo mechanistic studies demonstrating that BabA-mediated attachment can potentiate CagA translocation by the T4SS (16) and promote autoantibody-mediated gastritis, parietal cell loss, and mucosa-associated lymphoid tissue in Leb transgenic mice (17).…”

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confidence: 54%

Dynamic Expression of the BabA Adhesin and Its BabB Paralog during Helicobacter pylori Infection in Rhesus Macaques

et al. 2017

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Most Helicobacter pylori strains express the BabA adhesin, which binds to ABO/Leb blood group antigens on gastric mucin and epithelial cells and is found more commonly in strains that cause peptic ulcers or gastric cancer, rather than asymptomatic infection. We and others have previously reported that in mice, gerbils, and rhesus macaques, expression of babA is lost, either by phase variation or by gene conversion, in which the babB paralog recombines into the babA locus. The functional significance of loss of babA expression is unknown. Here we report that in rhesus monkeys, there is independent selective pressure for loss of babA and for overexpression of BabB, which confers a fitness advantage. Surprisingly, loss of babA by phase variation or gene conversion is not dependent on the capacity of BabA protein to bind Leb, which suggests that it may have other, unrecognized functions. These findings have implications for the role of outer membrane protein diversity in persistent H. pylori infection.

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confidence: 54%

Dynamic Expression of the BabA Adhesin and Its BabB Paralog during Helicobacter pylori Infection in Rhesus Macaques

et al. 2017

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“…It has been speculated for B. henselae that BadA and the VirB/D4 T4SS might interact synergistically in a way that BadA would mediate initial attachment to target cells, facilitate effector secretion, and manipulate cellular functions together with the Beps (322). The concept of such a relationship between an adhesin and a T4SS is reminiscent of the case for Helicobacter pylori, where host cell binding via the BabA protein was shown to amplify phenotypes associated with effector secretion (199). Although one could imagine that the enormous size and the dense surface layer of BadA may interfere with Bartonella effector secretion, the T-pilus of the planttargeting A. tumefaciens VirB/D4 T4SS is known to range from 1.4 m length on average up to even 4.5 m and would hence be much longer than BadA (8).…”

Section: The Primary Nichementioning

confidence: 96%

Intruders below the Radar: Molecular Pathogenesis of Bartonella spp

2012

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SUMMARY Bartonella spp. are facultative intracellular pathogens that employ a unique stealth infection strategy comprising immune evasion and modulation, intimate interaction with nucleated cells, and intraerythrocytic persistence. Infections with Bartonella are ubiquitous among mammals, and many species can infect humans either as their natural host or incidentally as zoonotic pathogens. Upon inoculation into a naive host, the bartonellae first colonize a primary niche that is widely accepted to involve the manipulation of nucleated host cells, e.g., in the microvasculature. Consistently, in vitro research showed that Bartonella harbors an ample arsenal of virulence factors to modulate the response of such cells, gain entrance, and establish an intracellular niche. Subsequently, the bacteria are seeded into the bloodstream where they invade erythrocytes and give rise to a typically asymptomatic intraerythrocytic bacteremia. While this course of infection is characteristic for natural hosts, zoonotic infections or the infection of immunocompromised patients may alter the path of Bartonella and result in considerable morbidity. In this review we compile current knowledge on the molecular processes underlying both the infection strategy and pathogenesis of Bartonella and discuss their connection to the clinical presentation of human patients, which ranges from minor complaints to life-threatening disease.

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“…The binding between babA and Le b antigen is important not only for H. pylori to adhere to the stomach surface but also to anchor the bacterial secretion system (T4SS) to the host cell surface so that bacterial factors, including the CagA protein, can be effectively injected into the host cell cytosol. This interaction plays an important role in potentiating T4SS-mediated secretion, resulting in inflammation and IM [47,51], although we cannot address how specifically blood group type A affects H. pylori attachment to gastric epithelial cells. Animal experiments revealed that babA could stimulate the inflammatory cells to release more IL-8, CCL5 pro-inflammatory cytokines, and precancer-related factors (CDX2 and MUC2) [51].…”

Section: Resultsmentioning

confidence: 99%

“…This interaction plays an important role in potentiating T4SS-mediated secretion, resulting in inflammation and IM [47,51], although we cannot address how specifically blood group type A affects H. pylori attachment to gastric epithelial cells. Animal experiments revealed that babA could stimulate the inflammatory cells to release more IL-8, CCL5 pro-inflammatory cytokines, and precancer-related factors (CDX2 and MUC2) [51]. Since inflammatory response to H. pylori infection plays an important role in cellular proliferation and gastric mucosal damage, the upregulation of pro-inflammatory cytokines in people with chronic gastritis may be an important clinical implication in gastric carcinogenesis.…”

Section: Resultsmentioning

confidence: 99%

Clinical Evaluation of Triple and Quadruple Helicobacter Pylori Eradication Therapy in Peptic Ulcer Patients With Different Abo Blood Group Phenotypes

Abdulridha

Kutaif

Kamal

et al. 2018

Asian J Pharm Clin Res

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Objective: This study aimed to examine the pathological changes in gastric mucosa of Helicobacter pylori-infected peptic ulcer patients carrying different ABO phenotypes and to study the response to the 14 days' standard triple therapy and 10 days' quadruple therapy in peptic ulcer patients according to their ABO phenotypes. Methods:Interventional prospective randomized-controlled open-label study was performed on newly diagnosed patients with PUD. The H. pyloripositive patients were allocated into two major study groups in which they are subdivided according to ABO blood group phenotypes: Group 1 received standard H. pylori eradication triple therapy and Group 2 received standard H. pylori eradication quadruple regimen. Patients were monitored after 2 months for successful H. pylori eradication.Results: Chronic active gastritis was significantly high in patients carrying blood Group O phenotype (81.25%), while the atrophic gastritis and intestinal metaplasia were significantly high in patients carrying blood Group A phenotype (25.00% and 16.67%), respectively. 14 days' triple therapy showed significantly lower eradication rate in H. pylori-infected peptic ulcer patients carrying blood Group O phenotype (p<0.01), meanwhile higher response was found among patients with blood Group B. 10 days' quadruple therapy produced a significant high eradication rate in H. pylori-infected patients carrying blood Group O than those with blood Group A (p<0.01), but still both showed lower response compared to that in patients carrying blood Group B and AB phenotypes. Elderly patients showed significantly less healing efficacy than younger patients (p<0.01), and the least healing rate was noticed in female patients after both regimens. Conclusion:Lower eradication rate in H. pylori-infected was noticed in peptic ulcer patients carrying blood Group O mainly than those with other blood groups and particularly those with duodenal Ulceri. 10 days' quadruple therapy showed significant higher eradication rate in H. pylori infection and a better ulcer healing efficacy.

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BabA-mediated Adherence Is a Potentiator of the Helicobacter pylori Type IV Secretion System Activity

Abstract: Chronic infection of

Cited by 165 publications

References 50 publications

Dynamic Expression of the BabA Adhesin and Its BabB Paralog during Helicobacter pylori Infection in Rhesus Macaques

Dynamic Expression of the BabA Adhesin and Its BabB Paralog during Helicobacter pylori Infection in Rhesus Macaques

Intruders below the Radar: Molecular Pathogenesis of Bartonella spp

Clinical Evaluation of Triple and Quadruple Helicobacter Pylori Eradication Therapy in Peptic Ulcer Patients With Different Abo Blood Group Phenotypes

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