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Helicobacter pylori infection is a well-established risk factor for the development of gastric cancer (GC). Understanding the immunopathogenesis underlying this association is crucial for developing effective preventive and therapeutic strategies. This narrative review comprehensively explores the immunopathogenesis of H. pylori-induced GC by delving into several key aspects, emphasizing the pivotal roles played by H. pylori virulence factors, including cytotoxin-associated gene A (cagA) and vacuolating cytotoxin A (vacA), blood group antigen-binding adhesin (babA), and sialic acid binding adhesin (sabA). Moreover, the review focuses on the role of toll-like receptors (TLRs) and cytokines in the complex interplay between chronic infection and gastric carcinogenesis. Finally, the study examines the association between H. pylori evasion of the innate and adaptive immune response and development of GC. A comprehensive understanding of the immunopathogenesis of H. pylori-induced GC is essential for designing targeted interventions to prevent and manage this disease. Further research is warranted to elucidate the intricate immune responses involved and identify potential therapeutic targets to improve patient outcomes.
Helicobacter pylori infection is a well-established risk factor for the development of gastric cancer (GC). Understanding the immunopathogenesis underlying this association is crucial for developing effective preventive and therapeutic strategies. This narrative review comprehensively explores the immunopathogenesis of H. pylori-induced GC by delving into several key aspects, emphasizing the pivotal roles played by H. pylori virulence factors, including cytotoxin-associated gene A (cagA) and vacuolating cytotoxin A (vacA), blood group antigen-binding adhesin (babA), and sialic acid binding adhesin (sabA). Moreover, the review focuses on the role of toll-like receptors (TLRs) and cytokines in the complex interplay between chronic infection and gastric carcinogenesis. Finally, the study examines the association between H. pylori evasion of the innate and adaptive immune response and development of GC. A comprehensive understanding of the immunopathogenesis of H. pylori-induced GC is essential for designing targeted interventions to prevent and manage this disease. Further research is warranted to elucidate the intricate immune responses involved and identify potential therapeutic targets to improve patient outcomes.
Background: This study aimed to determine the current EPIYA motifs of the cag A gene in Helicobacter pylori isolates from patients with gastric disorders, and evaluate the association between these patterns and the clinical outcome of H. pylori infection in different geographical regions of Iran. Materials and Methods: We examined 150 patients with gastrointestinal disorders from the central and eastern regions of Iran. The detection of H. pylori and screening of cag A was performed by polymerase chain reaction (PCR). The pattern of the motifs was determined by PCR followed by sequencing. Results: The overall prevalence of H. pylori was 66.3% in eastern (Mashad) and 50.6% in the central (Isfahan) part of Iran. The frequency of cag A-positive strains in Mashad and Isfahan were 63.4% and 56.7%, respectively. The pattern of EPIYA motif was as follows: 43 (79.6%) ABC, 7 (12.9%) AB, 4 (7.4%) ABCC, and one (1.9%) ABCCC. We also identified a novel EPIYA C sequence motif which showed association with gastric cancer (GC). The relationship between the frequency of specific EPIYA motifs and GC was statistically significant ( P < 0.05). Conclusions: This is the first report for the determination of the cag A EPIYA motif of H. pylori in the Northeast and center of Iran. The prevalence of cag A positive H. pylori between the two regions was significant ( P ≤ 0.05). All isolates of the H. pylori cag A were western type (ABC). The increase in the number of EPIYA-C repeats was associated with GC ( P ≤ 0.01).
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