Association between Helicobacter pylori genotypes and severity of chronic gastritis, peptic ulcer disease and gastric mucosal interleukin-8 levels: Evidence from a study in the Middle East.

Iqbal Siddique,Thamradeen A Junaid,Waleed Alazmi,Asmaa Al-Qabandi,Jaber Al-Ali,Abu Salim Mustafa,Anjum Memon

doi:10.1186/s13099-014-0041-1

Iqbal Siddique, Thamradeen A Junaid + Show 5 more

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https://doi.org/10.1186/s13099-014-0041-1

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Abstract

BackgroundThe varied clinical presentations of Helicobacter pylori (H. pylori) infection are most likely due to differences in the virulence of individual strains, which determines its ability to induce production of interleukin-8 (IL-8) in the gastric mucosa. The aim of this study was to examine association between cagA, vacA-s1 and vacA-s2 genotypes of H. pylori and severity of chronic gastritis and presence of peptic ulcer disease (PUD), and to correlate these with IL-8 levels in the gastric mucosa.MethodsGastric mucosal biopsies were obtained from patients during esophagogastroduodenoscopy. The severity of chronic gastritis was documented using the updated Sydney system. H. pylori cagA and vacA genotypes were detected by PCR. The IL-8 levels in the gastric mucosa were measured by ELISA.ResultsH. pylori cagA and/or vacA genotypes were detected in 99 patients (mean age 38.4±12.9; 72 males), of whom 52.5% were positive for cagA, 44.4% for vacA-s1 and 39.4% for vacA-s2; and 70.7% patients had PUD. The severity of inflammation in gastric mucosa was increased with vacA-s1 (p=0.017) and decreased with vacA-s2 (p=0.025), while cagA had no association. The degree of neutrophil activity was not associated with either cagA or vacA-s1, while vacA-s2 was significantly associated with decreased neutrophil activity (p=0.027). PUD was significantly increased in patients with cagA (p=0.002) and vacA-s1 (p=0.031), and decreased in those with vacA-s2 (p=0.011). The level of IL-8 was significantly increased in patients with cagA (p=0.011) and vacA-s1 (p=0.024), and lower with vacA-s2 (p=0.004). Higher levels of IL-8 were also found in patients with a more severe chronic inflammation (p=0.001), neutrophil activity (p=0.007) and those with PUD (p=0.001).ConclusionsPresence of vacA-s1 genotype of H. pylori is associated with more severe chronic inflammation and higher levels of IL-8 in the gastric mucosa, as well as higher frequency of PUD. Patients with vacA-s2 have less severe gastritis, lower levels of IL-8, and lower rates of PUD. The presence of cagA genotype is not associated with the severity of gastritis or IL-8 induction in the gastric mucosa. The association of cagA with PUD may be a reflection of its presence with vacA-s1 genotype.

Highlights

The varied clinical presentations of Helicobacter pylori (H. pylori) infection are most likely due to differences in the virulence of individual strains, which determines its ability to induce production of interleukin-8 (IL-8) in the gastric mucosa
H. pylori were seen on histopathology in 98 of these patients, all of whom were positive for cagA and/or vacuolating cytotoxin A (vacA)
In our study both the degree of chronic inflammation and neutrophil activity in the gastric mucosa were more severe in patients who were infected with H. pylori containing the cagA and vacA-s1 genes

Summary

Introduction

The varied clinical presentations of Helicobacter pylori (H. pylori) infection are most likely due to differences in the virulence of individual strains, which determines its ability to induce production of interleukin-8 (IL-8) in the gastric mucosa. The aim of this study was to examine association between cagA, vacA-s1 and vacA-s2 genotypes of H. pylori and severity of chronic gastritis and presence of peptic ulcer disease (PUD), and to correlate these with IL-8 levels in the gastric mucosa. Helicobacter pylori (H. pylori) colonizes the mucosa of the human stomach and establishes a long-term infection [1] It leads to the development of chronic gastritis, peptic ulcer disease (PUD), mucosal-associated lymphoid tissue (MALT) lymphoma and gastric carcinoma [2,3]. The cagA gene is not present in every H. pylori strain, but is associated with more severe clinical results such as more severe inflammation of the gastric mucosa, as well as higher prevalence of PUD and gastric carcinoma [8,9,10]. The vacA-s1 strains are associated with more severe gastric inflammation and PUD independently of cagA, while vacA-s2 strains are associated with lower ulcer prevalence and less severe inflammation [14]

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