Helicobacter pylori and IL-8 Signaling: Implications in Gastritis and Peptic Ulcer Disease

Abstract

The gram-negative spiral bacterium Helicobacter pylori has many flagella to colonize the stomach mucosa. Urease neutralizes stomach acid and helps H. pylori survive. Warren and Marshall found that H. pylori causes chronic gastritis, peptic ulcer disease (PUD), gastric cancer, and mucosa-associated lymphoid tissue lymphoma. H. pylori infects 50% of the worldwide population, although only a portion develops gastroduodenal diseases due to bacterial virulence, host genetics, and environmental variables.   CagA and VacA, which harm epithelial cells and stimulate the immune system, are the main virulence factors. Interleukin-8 (IL-8), a pro-inflammatory cytokine that attracts neutrophils and T cells, is released by the stomach epithelium, worsening tissue inflammation and ulcer development. The IL-8 -251 polymorphism (rs4073) increases IL-8 production and increases the risk of gastritis, peptic ulcer disease, and stomach malignancies.   Bacterial virulence, host immune responses, and genetic variations are key to H. pylori-related diseases. IL-8 is crucial to stomach mucosal inflammation and may be a biomarker for H. pylori disease susceptibility and progression.