| Summary: | <i>Background:</i> <i>Helicobacter pylori</i> 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 <i>Helicobacter pylori</i> patients with gastric intestinal metaplasia and dysplasia (IM/DYS). We also investigated the serum IL-17A levels in <i>Helicobacter pylori</i> patients with gastric intestinal metaplasia and dysplasia, and patients with <i>Helicobacter pylori</i> non-atrophic gastritis (NAG). <i>Methods:</i> the IL-17 cytokine profile of gastric T cells was investigated in six patients with IM/DYS and <i>Helicobacter pylori</i> infection. Serum IL-17A levels were measured in 45 <i>Helicobacter pylori</i>-infected IM/DYS patients, 45 <i>Helicobacter pylori</i>-infected patients without IM/DYS and in 45 healthy controls (HC). <i>Results:</i> gastric T cells from all IM/DYS patients with <i>Helicobacter pylori</i> were able to proliferate in response to <i>Helicobacter pylori</i> and to produce IL-17A. The Luminex analysis revealed that IL-17A levels were significantly increased in <i>Helicobacter pylori</i> IM/DYS patients compared to healthy controls and to <i>Helicobacter pylori</i> gastritis patients without IM/DYS (452.34 ± 369.13 pg/mL, 246.82 ± 156.06 pg/mL, 169.26 ± 73.82 pg/mL, respectively; <i>p</i> < 0.01, <i>p</i> < 0.05). <i>Conclusions:</i> the results obtained indicate that <i>Helicobacter pylori</i> is able to drive gastric IL-17 inflammation in IM/DYS <i>Helicobacter pylori</i>-infected patients, and that IL-17A serum levels are significantly increased in <i>Helicobacter pylori</i>-infected patients with IM/DYS.
|
|---|