Helicobacter pylori Infection Synergistic with IL-1β Gene Polymorphisms Potentially Contributes to the Carcinogenesis of Gastric Cancer

• Published in: International journal of medical sciences 2016-01, Vol.13 (4), p.298-303
• Main Authors: Hong, Jun-Bo, Zuo, Wei, Wang, An-Jiang, Lu, Nong-Hua
• Format: Article
• Language: English
• Subjects: Alleles; Carcinogenesis - genetics; Gastric Mucosa - microbiology; Gastric Mucosa - pathology; Genotype; Helicobacter Infections - genetics; Helicobacter Infections - microbiology; Helicobacter Infections - pathology; Helicobacter pylori - genetics; Helicobacter pylori - pathogenicity; Humans; Interleukin-1beta - biosynthesis; Interleukin-1beta - genetics; Polymorphism, Genetic; Review; Stomach Neoplasms - genetics; Stomach Neoplasms - microbiology; Stomach Neoplasms - pathology
• ISSN: 1449-1907; 1449-1907
• DOI: 10.7150/ijms.14239

Helicobacter pylori (H. pylori) infection is the most common chronic bacterial infection in the world and the etiological agent for most gastric cancer (GC). Interleukin-1β (IL-1β) is a potent proinflammatory cytokine, and its deregulation is closely associated with the tumorigenesis of several cancers. Recent studies have revealed that the IL-1β-31 and -511T alleles are closely associated with gastric carcinogenesis due to their roles in the induction of gastric precancerous lesions and hypochlorhydria. Furthermore, H. pylori infection has a synergistic effect on the development of GC with IL-1β gene polymorphisms, and the highest prevalence of severe gastric abnormalities are found in patients with both host and bacterial high-risk genotypes (cagA(+)/vacAs1(+)/IL-1β-511T). Therefore, these recent advances demonstrate that H. pylori synergistic with IL-1β gene polymorphisms contribute to the gastric carcinogenesis by their involvement in precancerous gastric lesions and low gastric acid secretion.