Host pathogen interactions in Helicobacter pylori related gastric cancer
Magdalena Chmiela1, Zuzanna Karwowska1, Weronika Gonciarz1
1Magdalena Chmiela, Weronika Gonciarz, Bujana Allushi, Department of Immunology and Infectious Biology, Institute of Microbiology, Biotechnology and Immunology, Faculty of Biology and Environmental Protection, University of Lodz, Banacha, 90-237 Lodz, Poland.
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.
Insights
Helicobacter pylori (H. pylori) infection is a major cause of gastric cancer worldwide. This common bacterial pathogen can lead to severe stomach conditions, underscoring the need for early detection and treatment.
Area of Science:
- Microbiology and Pathogenesis
- Gastroenterology and Oncology
Background:
- Helicobacter pylori (H. pylori) is a gram-negative bacterium colonizing the human stomach, infecting nearly half the global population.
- H. pylori infection is a confirmed cause of gastritis, peptic ulcers, gastric cancer, and MALT lymphoma.
Discussion:
- Individual susceptibility to H. pylori-induced diseases is multifactorial, involving bacterial virulence, host genetics, and immune response.
- H. pylori is a Group I carcinogen, responsible for a significant portion of cancer-related deaths, particularly gastric cancer.
- Chronic infection leads to genetic instability in gastric cells and impaired DNA repair, promoting malignancy.
Key Insights:
- H. pylori infection is a significant risk factor for both intestinal-type and diffuse gastric cancer.
- Host genetic factors, including gene polymorphisms related to inflammation and cytokine response, influence disease outcomes.
- Bacterial strains vary in their capacity to trigger detrimental inflammatory responses that promote cancer development.
Outlook:
- Early detection of gastric cancer, often asymptomatic in initial stages, is crucial for improving survival rates.
- Understanding H. pylori's role in carcinogenesis necessitates continued research into eradication and prevention strategies.
- H. pylori should be recognized as a critical pro-cancerous factor in clinical and research settings.
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