Helicobacter pylori infection is one of the most common bacterial infections in the world. It is responsible for most cases of chronic gastritis and peptic ulcer disease, and the main risk factor for gastric cancers (adenocarcinoma and gastric mucosa-associated lymphoid tissue lymphoma). Recent studies suggest an increased H. pylori prevalence in patients with various extra gastrointestinal disorders, including skin, cardiovascular, rheumatic, liver diseases and respiratory disorders, including chronic obstructive pulmonary disease (COPD), bronchiectasis and active pulmonary tuberculosis. The observed associations might be explained by a potential etiopathogenetic role of H. pylori infection in these disorders. Estimates suggest that half the world is infected with the bacteria, with an especially high rate of infection in Asia. We know that H. pylori causes ulcers, but do all strains of H. pylori cause ulcers and why some people experience symptoms while others remain asymptomatic? If we can understand that we may be more efficient at treating and avoiding development of H. pylori antibiotic resistance. Helicobacter pylori are a spiralshaped, microaerophilic and Gram-negative bacterium discovered by Marshall and Warren. This bacterium possesses strain-specific virulence factors cytotoxin associated gene A (CagA) and vacuolating cytotoxin gene A (VacA) that allow the organism to colonize the gastric mucosa, evade host defense and, finally, damage host tissue. H. pylori colonization of the gastric mucosa stimulates the release of a variety of proinflammatory cytokines, including interleukin (IL)-1, IL-8 and tumor necrosis factor-α. Moreover, a crossmolecular mimicry between bacterial and host antigens exists in H. pylori-infected patients. Therefore, H. pylori might have a pathogenetic role in diseases characterized by abnormal activation of inflammatory mediators and/ or induction of autoimmunity.