This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research article
Santiago Escalante
Pontificia Universidad Catolica del Ecuador
Corresponding Author
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Summary
Background
Helicobacter pylori is the main microorganism causing gastrointestinal diseases, such as chronic gastritis, peptic ulcer, MALT lymphoma, among others. The presence of the s1/m1 genotype of the vacA gene and EPIYA phosphorylation motifs of the cagA gene have been linked to the production of prolonged gastric inflammation. This study determines the presence of these virulence genotypes and their relationship with atrophic gastritis.
Methods
We included 231 patients with a history of dyspepsia undergoing upper gastrointestinal endoscopy. Samples of gastric tissue were taken to establish, through molecular techniques, the presence of H. pylori by amplifying the ureA and flaA2 housekeeping genes; in addition, the alleles of signal (s) and of the middle region (m) present in the vacA gene were amplified; and by sequencing the repeating patterns of the tyrosine phosphorylation motifs within the Glu-Pro-Ile-Tyr-Ala (EPIYA) motifs of the cagA gene were also amplified. A chi-square test was performed in order to establish the relationship between the virulence genes and the degrees of gastric injury.
Results
A total of (91/231) samples were positive for H. pylori, of which (57/91) amplified the cagA gene and (66/91) the vacA gene. 81.8% (54/66) of the positive samples for the vacA gene showed the combination of the s1/m1 alleles, associated mostly with atrophic gastritis (AG). The most frequent EPIYA motifs were ABC and ABCC, with 54.4% (31/57) and 40.4% (23/57) respectively. A relation of the genes with AG and its injury severity with a p>0.05 value was observed. The cagA +/vacA s1/m1+/EPIYA ABC pattern is found in most samples. A p=0.02 relationship was found between the presence of the vacA gene and the cagA gene.
Conclusions
The results show a higher proportion of gastric atrophy in patients infected with H. pylori. The sum of the pathogenicity factors such as the cagA+/vacA s1/m1+/EPIYA ABCC genotype increases the virulence potential of the microorganism, suggesting that the coexistence of these genes could result in an increase in the severity of the progression of inflammation that leads to precancerous lesions.
Keywords
Helicobacter pylori, Atrophic Gastritis, Intestinal Metaplasia, vacA, caGA, EPIYA motifs.
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This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research article
Santiago Escalante
Pontificia Universidad Catolica del Ecuador
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 10 Jul, 2019
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Summary
Background
Helicobacter pylori is the main microorganism causing gastrointestinal diseases, such as chronic gastritis, peptic ulcer, MALT lymphoma, among others. The presence of the s1/m1 genotype of the vacA gene and EPIYA phosphorylation motifs of the cagA gene have been linked to the production of prolonged gastric inflammation. This study determines the presence of these virulence genotypes and their relationship with atrophic gastritis.
Methods
We included 231 patients with a history of dyspepsia undergoing upper gastrointestinal endoscopy. Samples of gastric tissue were taken to establish, through molecular techniques, the presence of H. pylori by amplifying the ureA and flaA2 housekeeping genes; in addition, the alleles of signal (s) and of the middle region (m) present in the vacA gene were amplified; and by sequencing the repeating patterns of the tyrosine phosphorylation motifs within the Glu-Pro-Ile-Tyr-Ala (EPIYA) motifs of the cagA gene were also amplified. A chi-square test was performed in order to establish the relationship between the virulence genes and the degrees of gastric injury.
Results
A total of (91/231) samples were positive for H. pylori, of which (57/91) amplified the cagA gene and (66/91) the vacA gene. 81.8% (54/66) of the positive samples for the vacA gene showed the combination of the s1/m1 alleles, associated mostly with atrophic gastritis (AG). The most frequent EPIYA motifs were ABC and ABCC, with 54.4% (31/57) and 40.4% (23/57) respectively. A relation of the genes with AG and its injury severity with a p>0.05 value was observed. The cagA +/vacA s1/m1+/EPIYA ABC pattern is found in most samples. A p=0.02 relationship was found between the presence of the vacA gene and the cagA gene.
Conclusions
The results show a higher proportion of gastric atrophy in patients infected with H. pylori. The sum of the pathogenicity factors such as the cagA+/vacA s1/m1+/EPIYA ABCC genotype increases the virulence potential of the microorganism, suggesting that the coexistence of these genes could result in an increase in the severity of the progression of inflammation that leads to precancerous lesions.
Figure 1
Figure 2
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