| First Author | Shigematsu Y | Year | 2013 |
| Journal | Cancer Lett | Volume | 340 |
| Issue | 1 | Pages | 141-7 |
| PubMed ID | 23920123 | Mgi Jnum | J:204372 |
| Mgi Id | MGI:5532423 | Doi | 10.1016/j.canlet.2013.07.034 |
| Citation | Shigematsu Y, et al. (2013) Interleukin-1beta induced by Helicobacter pylori infection enhances mouse gastric carcinogenesis. Cancer Lett 340(1):141-7 |
| abstractText | Interleukin-1beta (Il1b) is considered to be involved in Helicobacter pylori (HP)-induced human gastric carcinogenesis, while the role of its polymorphisms in gastric cancer susceptibility remains controversial. Here, we aimed to clarify the role of HP infection-induced IL1B in gastric inflammation and carcinogenesis using Il1b(-/-) (Il1b-null) mice. In gastric mucosa of the Il1b(+/+) (WT) mice, HP infection induced Il1b expression and severe inflammation. In contrast, in Il1b-null mice, recruitment of neutrophils and macrophages by HP infection was markedly suppressed. In a carcinogenicity test, the multiplicity of gastric tumors was significantly suppressed in theIl1b-null mice (58% of WT; P<0.005). Mechanistically, HP infection induced NF-kappaB activation both in the inflammatory and epithelial cells in gastric mucosae, and the activation was attenuated in the Il1b-null mice. Accordingly, increased proliferation and decreased apoptosis of gastric epithelial cells induced by HP infection in the WT mice were attenuated in the Il1b-null mice. These results demonstrated that the IL1B physiologically induced by HP infection enhanced gastric carcinogenesis by affecting both inflammatory and epithelial cells. |
