What is Helicobacter pylori infection?
Helicobacter pylori (H. pylori) infection is a bacterial infection that primarily affects the stomach and the upper part of the small intestine (duodenum). It is one of the most common bacterial infections worldwide, with prevalence varying by geographical region and socioeconomic factors. H. pylori infection is usually acquired during childhood and can persist for many years if left untreated.
- pylori is a spiral-shaped bacterium that colonizes the mucous layer of the stomach lining, where it can evade the body’s immune response and establish a chronic infection. The exact route of transmission of H. pylori is not entirely clear, but it is believed to be spread through oral-oral or fecal-oral routes, such as through contaminated food, water, or close contact with an infected individual.
What is the relationship between Helicobacter pylori infection and oxidative stress?
The relationship between Helicobacter pylori (H. pylori) infection and oxidative stress involves complex interactions between the bacterium, the host immune response, and the generation of reactive oxygen species (ROS) within the gastric mucosa. Oxidative stress refers to an imbalance between the production of ROS and the body’s antioxidant defenses, leading to cellular damage and dysfunction. Several mechanisms contribute to oxidative stress in the context of H. pylori infection:
- Induction of Inflammatory Response: pylori infection triggers a robust inflammatory response in the gastric mucosa, characterized by the infiltration of immune cells, release of pro-inflammatory cytokines, and activation of inflammatory pathways. The inflammatory cascade generates ROS as byproducts of immune cell activation and respiratory burst reactions, leading to oxidative stress within the gastric epithelium.
- Production of Reactive Oxygen Species by pylori: H. pylori itself can produce ROS as part of its normal metabolic processes. The bacterium produces enzymes such as urease and catalase, which generate ROS as byproducts of their enzymatic activities. These ROS can damage the gastric epithelium and contribute to oxidative stress within the gastric mucosa.
- Disruption of Antioxidant Defenses: pylori infection can disrupt the antioxidant defenses of the gastric mucosa, leading to impaired scavenging of ROS and increased susceptibility to oxidative damage. The bacterium can interfere with host antioxidant mechanisms by downregulating antioxidant enzymes such as superoxide dismutase (SOD), catalase, and glutathione peroxidase, which normally neutralize ROS and protect against oxidative stress.
- DNA Damage and Cellular Injury: Oxidative stress induced by pylori infection can cause damage to DNA, proteins, lipids, and other cellular components within the gastric mucosa. ROS can directly damage DNA and induce mutations, leading to genomic instability and increased risk of gastric carcinogenesis. Oxidative damage to proteins and lipids can disrupt cellular function and integrity, contributing to tissue injury and inflammation.
- Role in Gastric Carcinogenesis: Chronic pylori infection and associated oxidative stress have been implicated in the development of gastric cancer. Prolonged exposure to ROS and reactive nitrogen species (RNS) can lead to DNA damage, activation of oncogenic signaling pathways, and promotion of tumor growth and progression. Oxidative stress-induced genomic instability and DNA damage contribute to the accumulation of genetic alterations and malignant transformation of gastric epithelial cells.
Overall, oxidative stress plays a significant role in the pathogenesis of H. pylori-associated gastric diseases, including gastritis, peptic ulcers, and gastric cancer.