Association Between Helicobacter pylori cagA, babA2 Virulence Factors and Gastric Mucosal Interleukin-33 mRNA Expression and Clinical Outcomes in Dyspeptic Patients

Helicobacter pylori (H. pylori) infection has been reported in more than half of the world human population. It is
associated with gastric inflammation and noticeable infiltration of the immune cells to the stomach mucosa by
several cytokines secretion. IL-1β, IL-18 have been shown to contribute to H. pylori induced gastritis, but the
details of inflammation and association of virulence factors remain unclear. IL-1 cytokine family has a new
additional cytokine, Interleukin-33 (IL-33), which is contemplated to have an important role for host defense
against microorganisms. H. pylori virulence factors important in gastritis risk are the cag pathogenicity island
(cag-PAI) and babA. This study evaluated IL-33 mucosal mRNA expression levels in infected and uninfected
patients and its relationship with bacterial virulence factors cagA, babA2 and type of gastritis. Total RNA was extracted from gastric biopsies of 79 H. pylori-infected patients and 51 H. pylori-negative patients. Mucosal IL-
33 mRNA expression levels in gastric biopsies were assessed using real-time PCR. Existence of virulence
factors were detected by PCR. IL-33 mRNA expression was significantly higher in biopsies of H. pylori-infected
patients compared to H. pylori-uninfected patients (P<0.0001). Also there was a direct relationship between
virulence factor bab-A2 and enhancement in IL-33 mRNA expression. Furthermore, IL-33 mRNA expression
level was significantly lower in chronic gastritis patients compared with patients with active gastritis (P<0.001).
IL-33 may play a crucial role in the inflammatory response and induction of the chronic gastritis and severity of
inflammatory changes in the gastric mucosa.