REVIEW ON STIMULATIONS OF THE SPREAD OF HELICOBACTER PYLORI INFECTION IN IRAQ

Abstract

Helicobacter pylori (H. pylori) bacteria are microaerophilic Gram-negative bacteria that inhabit the human stomach and duodenum. If left untreated, it can lead to prolonged infection in human life. Numerous studies have shown that H. pylori infection can cause several important gastrointestinal diseases, ranging from chronic active gastritis without clinical symptoms to peptic ulcer, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue lymphoma. Most modern publications are devoted to the pathogenic properties of microorganisms in the development of chronic gastritis, gastric ulcers, and gastric cancer, and methods for their eradication. Helicobacter pylori was the first officially recognized bacterial carcinogen and one of the most successful human pathogens, as more than half of the world's population is colonized by this Gram-negative bacterium. The disease course is the result of complex interactions between the host and bacteria. Host immunity gene polymorphisms and gastric acid secretion largely determine the ability of bacteria to colonize specific gastric niches. Bacterial virulence factors such as the cytotoxin-related gene pathogenicity island-encoded protein CagA and the vacuolar cytotoxin VacA support this colonization of the gastric mucosa and subsequently appear to regulate the host's immune system. This study focuses on the microbiological, clinical, and immunological aspects of H. pylori pathogenesis; it also reveals the prevalence of H. pylori in some Iraqi governorates