Helicobacter pylori infection causes both protective and deleterious effects in human health and disease

Abstract

Infection with Helicobacter pylori (H. pylori) is necessary but not sufficient for the development of gastric cancer, the third leading cause of cancer death globally. H. pylori infection affects over half of people globally; however, it does not affect populations uniformly. H. pylori infection rates are declining in western industrialized countries but are plateauing in developing and newly industrialized countries where gastric cancer is most prevalent. Despite H. pylori infection being the primary causative agent for gastric cancer, H. pylori infection can also cause other effects, detrimental or beneficial, throughout an individual's life, with the beneficial effects often being seen in childhood and the deleterious effects in adulthood. H. pylori is an ancient bacterium and its likelihood of affecting disease or health is dependent on both human and bacterial genetics that have co-evolved over millennia. In this review, we focus on the impact of infection and its genetic bases in different populations and diseases throughout an individual's lifespan, highlighting the benefits of individualized treatment and argue that universal eradication of H. pylori in its host may cause more harm than good for those infected with H. pylori.

Figure 1:. Global distribution of H. pylori and Gastric Cancer.

The prevalence of H. pylori infection as percent of total adult population (A), gastric cancer incidence presented as number per 100,000 (B) mapped with the most recent H. pylori prevalence data(5) and gastric cancer incidence rates from the WHO except where WHO did not have data, in which case data was supplemented from recent publications or presented as no data available (in gray) (–103). As gastric cancer incidence is generally presented for male and females separately we took average of the two for the figures. The average for each country is presented. The locales of the three gastric cancer enigmas, the African Enigma, the Asian Enigma, and the Latin America High Altitude Enigma (C), highlighting the contrast of H. pylori infection incidence and gastric cancer prevalence.

Figure 2:. H. pylori colonization.

H. pylori enters the stomach, and the urease activity reduces the acidity of the local environment. The H. pylori flagella-mediated motility facilitate its movement towards the lower mucosa, and it enters the epithelium with assistance from several adhesins including babA and sabA. Once the epithelium is successfully colonized, H. pylori release toxins including cagA and vacA. The figure modified from Kao et al (12).