Pathogenicity of Helicobacter pylori infection

Radosz-Komoniewska, Halina; Bek, T.; Jóźwiak, Jarosław; Martirosian, Gayane

doi:10.1111/j.1469-0691.2005.01207.x

Cited by 39 publications

(36 citation statements)

References 65 publications

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“…However, KILTZ et al (13) did not observe the development of reflux esophagitis for those cured of the H. pylori infection, even if infected by CagA-positive strains. Another Brazilian study, by QUEIROZ et al (32) has provided evidence supporting the independent protective roles of CagA-positive H. pylori strains and the degree of corpus gastritis against GERD. When the CagA genotypes were analyzed, no statistically significant differences were found among the samples collected from the corpus and those from the antrum.…”

Section: Discussionmentioning

confidence: 99%

Neither genotype nor the gastric colonization site of Helicobacter pylori are predictive factors for the development of erosive esophagitis in patients with peptic ulcer disease, 1 year after eradication

Batista

Silva

Eisig

et al. 2009

Arq. Gastroenterol.

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-Context -WhetherHelicobacter pylori infection is a protective or predisposing factor for the development of gastroesophageal reflux disease remains controversial. The most virulent strains, such as those expressing the cytotoxin-associated gene A (CagA), and the site of gastric colonization have been correlated with the prevention or development of esophagitis. Aim -To determine the incidence of erosive esophagitis following eradication of H. pylori in patients with peptic ulcer disease and to evaluate the association of erosive esophagitis with virulent strains of H. pylori and the site of gastric colonization. Methods -Triple therapy with lansoprazole, amoxicillin and clarithromycin was administered to 159 patients with peptic ulcer disease. Endoscopy, histopathology, urease and carbon-14 urea breath tests were performed prior to treatment, at 3 months and 1 year following treatment. Genotyping of H. pylori strains using polymerase chain reaction was performed separately on samples from the corpus and antrum. Results -One year after treatment, 148 successfully treated patients were reevaluated. Twenty-eight patients (19%) had erosive esophagitis, classified as Los Angeles grade A in 24 and B in 4. The samples taken from the corpus were CagA-positive in 18 patients (64%), while the samples taken from the antrum were CagA-positive in 21 patients (75%). Conclusions -The incidence of erosive esophagitis in peptic ulcer patients who had their H. pylori eradicated was 19%. No correlation was found between the gastric site colonized by H. pylori or strains expressing CagA and the prevention or development of erosive esophagitis in patients with peptic ulcer disease, 1 year after infection eradication. HEADINGS -Helicobacter pylori. Peptic ulcer. Esophagitis.

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Section: Discussionmentioning

confidence: 99%

Neither genotype nor the gastric colonization site of Helicobacter pylori are predictive factors for the development of erosive esophagitis in patients with peptic ulcer disease, 1 year after eradication

Batista

Silva

Eisig

et al. 2009

Arq. Gastroenterol.

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“…The pathogenesis of H. pylori infection is complex, and additional pathogenic factors, host factors, and their intramolecular cross talk continue to be discovered (18,(42)(43)(44)(45)(46)(47). Although H. pylori infection causes chronic gastric inflammation, the immune escape of H. pylori infection, particularly under high levels of IFN-g, has been less commonly reported.…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori Infection Activates Src Homology-2 Domain–Containing Phosphatase 2 To Suppress IFN-γ Signaling

Wang

Chen

Sheu

et al. 2014

The Journal of Immunology

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Helicobacter pylori infection not only induces gastric inflammation but also increases the risk of gastric tumorigenesis. IFN-γ has antimicrobial effects; however, H. pylori infection elevates IFN-γ–mediated gastric inflammation and may suppress IFN-γ signaling as a strategy to avoid immune destruction through an as-yet-unknown mechanism. This study was aimed at investigating the mechanism of H. pylori–induced IFN-γ resistance. Postinfection of viable H. pylori decreased IFN-γ–activated signal transducers and activators of transcription 1 and IFN regulatory factor 1 not only in human gastric epithelial MKN45 and AZ-521 but also in human monocytic U937 cells. H. pylori caused an increase in the C-terminal tyrosine phosphorylation of Src homology-2 domain–containing phosphatase (SHP) 2. Pharmacologically and genetically inhibiting SHP2 reversed H. pylori–induced IFN-γ resistance. In contrast to a clinically isolated H. pylori strain HP238, the cytotoxin-associated gene A (CagA) isogenic mutant strain HP238CagAm failed to induce IFN-γ resistance, indicating that CagA regulates this effect. Notably, HP238 and HP238CagAm differently caused SHP2 phosphorylation; however, imaging and biochemical analyses demonstrated CagA-mediated membrane-associated binding with phosphorylated SHP2. CagA-independent generation of reactive oxygen species (ROS) contributed to H. pylori–induced SHP2 phosphorylation; however, ROS/SHP2 mediated IFN-γ resistance in a CagA-regulated manner. This finding not only provides an alternative mechanism for how CagA and ROS coregulate SHP2 activation but may also explain their roles in H. pylori–induced IFN-γ resistance.

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“…A great number of these factors are highly immunogenic. Among the most intensively studied immunodominant antigens are CagA, which, upon injection into eukaryotic cells, subverts the cellular functions; proteins responsible for cell motility, urease subunits, which allow the bacterium to survive in acidic environments; vacuolating toxin VacA, which is a potent inducer of epithelial cell apoptosis; neutrophil-activating protein NapA, CagF, and other proteins encoded by the pathogenicity island PAI; and some surface-located adhesins [2,9,27,42]. Initially, immunogenicity of these proteins was confirmed by classical molecular biology methods and one-dimensional (1-D) electrophoresis followed by Western blotting with antibodies raised in experimental animals or sera obtained from H. pylori-positive individuals with different gastroduodenal pathologies.…”

Section: Introductionmentioning

confidence: 99%

Tip-α (hp0596 Gene Product) Is a Highly Immunogenic Helicobacter pylori Protein Involved in Colonization of Mouse Gastric Mucosa

et al. 2008

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A product of the Helicobacter pylori hp0596 gene (Tip-a) is a highly immunogenic homodimeric protein, unique for this bacterium. Cell fractionation experiments indicate that Tip-a is anchored to the inner membrane. In contrast, the three-dimensional model of the protein suggests that Tip-a is soluble or, at least, largely exposed to the solvent. hp0596 gene knockout resulted in a significant decrease in the level of H. pylori colonization as measured by real-time PCR assay. In addition, the Tip-a recombinant protein was determined to stimulate macrophage to produce IL-1a and TNF-a. Both results imply that Tip-a is rather loosely connected to the inner membrane and potentially released during infection.

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Pathogenicity of Helicobacter pylori infection

Cited by 39 publications

References 65 publications

Neither genotype nor the gastric colonization site of Helicobacter pylori are predictive factors for the development of erosive esophagitis in patients with peptic ulcer disease, 1 year after eradication

Neither genotype nor the gastric colonization site of Helicobacter pylori are predictive factors for the development of erosive esophagitis in patients with peptic ulcer disease, 1 year after eradication

Helicobacter pylori Infection Activates Src Homology-2 Domain–Containing Phosphatase 2 To Suppress IFN-γ Signaling

Tip-α (hp0596 Gene Product) Is a Highly Immunogenic Helicobacter pylori Protein Involved in Colonization of Mouse Gastric Mucosa

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