Increased IL-17A Serum Levels and Gastric Th17 Cells in Helicobacter pylori-Infected Patients with Gastric Premalignant Lesions

Simple Summary Helicobacter pylori infection represents the major cause of gastric cancer, and is a type I carcinogen for distal gastric cancer. Gastric oncogenesis is a multi-step process and is related at least in part to a peculiar long-lasting gastric inflammation, which is still only partially understood. The aim of this study was to investigate which type of inflammation occurs in the stomach of Helicobacter pylori patients with gastric intestinal metaplasia and dysplasia, as well as to examine the serum levels of interleukin 17 in the same patients. We found that Helicobacter pylori is able to drive gastric IL-17 inflammation in gastric intestinal metaplasia and dysplasia in Helicobacter pylori-infected patients, and that IL-17A serum levels are significantly increased in patients with gastric intestinal metaplasia and dysplasia. We suggest that measurement of serum IL-17A might be useful for the management of Helicobacter pylori-infected patients, and eventually for predicting the development of gastric cancer. Background: Helicobacter pylori infection is characterized by an inflammatory infiltrate that might be an important antecedent of gastric cancer. The purpose of this study was to evaluate whether interleukin (IL)-17 inflammation is elicited by gastric T cells in Helicobacter pylori patients with gastric intestinal metaplasia and dysplasia (IM/DYS). We also investigated the serum IL-17A levels in Helicobacter pylori patients with gastric intestinal metaplasia and dysplasia, and patients with Helicobacter pylori non-atrophic gastritis (NAG). Methods: the IL-17 cytokine profile of gastric T cells was investigated in six patients with IM/DYS and Helicobacter pylori infection. Serum IL-17A levels were measured in 45 Helicobacter pylori-infected IM/DYS patients, 45 Helicobacter pylori-infected patients without IM/DYS and in 45 healthy controls (HC). Results: gastric T cells from all IM/DYS patients with Helicobacter pylori were able to proliferate in response to Helicobacter pylori and to produce IL-17A. The Luminex analysis revealed that IL-17A levels were significantly increased in Helicobacter pylori IM/DYS patients compared to healthy controls and to Helicobacter pylori gastritis patients without IM/DYS (452.34 +/- 369.13 pg/mL, 246.82 +/- 156.06 pg/mL, 169.26 +/- 73.82 pg/mL, respectively; p < 0.01, p < 0.05). Conclusions: the results obtained indicate that Helicobacter pylori is able to drive gastric IL-17 inflammation in IM/DYS Helicobacter pylori-infected patients, and that IL-17A serum levels are significantly increased in Helicobacter pylori-infected patients with IM/DYS.