Host pathogen interactions in Helicobacter pylori related gastric cancer

Abstract

Helicobacter pylori (H. pylori), discovered in 1982, is a microaerophilic, spiral-shaped gram-negative bacterium that is able to colonize the human stomach. Nearly half of the world's population is infected by this pathogen. Its ability to induce gastritis, peptic ulcers, gastric cancer and mucosa-associated lymphoid tissue lymphoma has been confirmed. The susceptibility of an individual to these clinical outcomes is multifactorial and depends on H. pylori virulence, environmental factors, the genetic susceptibility of the host and the reactivity of the host immune system. Despite the host immune response, H. pylori infection can be difficult to eradicate. H. pylori is categorized as a group I carcinogen since this bacterium is responsible for the highest rate of cancer-related deaths worldwide. Early detection of cancer can be lifesaving. The 5-year survival rate for gastric cancer patients diagnosed in the early stages is nearly 90%. Gastric cancer is asymptomatic in the early stages but always progresses over time and begins to cause symptoms when untreated. In 97% of stomach cancer cases, cancer cells metastasize to other organs. H. pylori infection is responsible for nearly 60% of the intestinal-type gastric cancer cases but also influences the development of diffuse gastric cancer. The host genetic susceptibility depends on polymorphisms of genes involved in H. pylori-related inflammation and the cytokine response of gastric epithelial and immune cells. H. pylori strains differ in their ability to induce a deleterious inflammatory response. H. pylori-driven cytokines accelerate the inflammatory response and promote malignancy. Chronic H. pylori infection induces genetic instability in gastric epithelial cells and affects the DNA damage repair systems. Therefore, H. pylori infection should always be considered a pro-cancerous factor.

Diminished circulating concentration of interleukin‐35 in Helicobacter pylori‐infected patients with peptic ulcer: Its association with FOXP3 gene polymorphism, bacterial virulence factor CagA, and gender of patients

“…Helicobacter pylori ( H. pylori ) is a bacterium with the ability to colonize the human stomach and is responsible for an infection which involves about half of the world's population . In developing and developed countries, the prevalence of H. pylori is about 80.0% and below 40.0%, respectively .…”

“…Helicobacter pylori ( H. pylori ) is a bacterium with the ability to colonize the human stomach and is responsible for an infection which involves about half of the world's population . In developing and developed countries, the prevalence of H. pylori is about 80.0% and below 40.0%, respectively . Long‐lasting infection and inflammation related to H. pylori lead to the peptic ulcer (PU) in about 15% to 20%, gastric mucosa‐associated lymphoid tissue (GALT) lymphoma in 0.1% to 3% and gastric cancer in less than 0.01% of the infected individuals .…”

“…Nevertheless, the most of H. pylori ‐infected individuals do not exhibit any gastrointestinal‐related clinical symptoms . The H. pylori ‐related virulence factors, the genetic background of the host and the reactivity of the immune system are the key factors in determining the clinical outcomes related to the H. pylori infection . The cytotoxin‐associated gene A (CagA) has been considered as an important virulence factor of the bacterium, showing a strong association with a more pronounced gastric inflammation and other gastrointestinal‐related clinical manifestations .…”

Unraveling the factors and mechanism involved in persistence: Host‐pathogen interactions in Helicobacter pylori

“…41,43 Overall, these results suggested that chemotaxis is a very important phenomenon that allows H. pylori to colonize in a special anatomical niche and persisting within the mid-gland. 44…”

“…In case of ChePep mutant strains, which colonize on the mucus layer similar to wild‐type strains, ΔChePep mutant is not colonized in the glandular region, which needs the bacterial movement . Overall, these results suggested that chemotaxis is a very important phenomenon that allows H. pylori to colonize in a special anatomical niche and persisting within the mid‐gland …”