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

doi:10.1186/s13099-014-0041-1

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

Gut Pathog. 2014 Sep 26;6(1):41. doi: 10.1186/s13099-014-0041-1. eCollection 2014.

Authors

Iqbal Siddique¹, Asmaa Al-Qabandi², Jaber Al-Ali³, Waleed Alazmi¹, Anjum Memon⁴, Abu Salim Mustafa⁵, Thamradeen A Junaid²

Affiliations

¹ Department of Medicine, Faculty of Medicine, Kuwait University, P. O. Box 24923, 13110 Safat, Kuwait ; Thunayan Al-Ghanim Gastroenterology Center, Al-Amiri Hospital, Sharq, Kuwait.
² Department of Pathology, Faculty of Medicine, Kuwait University, Jabriya, Kuwait.
³ Department of Medicine, Faculty of Medicine, Kuwait University, P. O. Box 24923, 13110 Safat, Kuwait.
⁴ Division of Primary Care and Public Health, Brighton and Sussex Medical School, Brighton, UK.
⁵ Department of Microbiology, Faculty of Medicine, Kuwait University, Jabriya, Kuwait.

Abstract

Background: 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.

Methods: Gastric 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.

Results: H. 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).

Conclusions: Presence 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.

Keywords: Gastritis; Helicobacter pylori; Interleukin-8; Peptic ulcer disease; cagA; vacA-s1; vacA-s2.