Interleukin-1β induced by Helicobacter pylori infection enhances mouse gastric carcinogenesis

Yasuyuki Shigematsu; Tohru Niwa; Emil Rehnberg; Takeshi Toyoda; Satoshi Yoshida; Akiko Mori; Mika Wakabayashi; Yoichiro Iwakura; Masao Ichinose; Yong Joon Kim; Toshikazu Ushijima

doi:10.1016/j.canlet.2013.07.034

Interleukin-1β induced by Helicobacter pylori infection enhances mouse gastric carcinogenesis

Yasuyuki Shigematsu, Tohru Niwa, Emil Rehnberg, Takeshi Toyoda, Satoshi Yoshida, Akiko Mori, Mika Wakabayashi, Yoichiro Iwakura, Masao Ichinose, Yong Joon Kim, Toshikazu Ushijima

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Abstract

Interleukin-1β (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 the. Il1b-null mice (58% of WT; P<. 0.005). Mechanistically, HP infection induced NF-κB 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.

Original language	English
Pages (from-to)	141-147
Number of pages	7
Journal	Cancer Letters
Volume	340
Issue number	1
DOIs	https://doi.org/10.1016/j.canlet.2013.07.034
Publication status	Published - 2013 Oct 28

Bibliographical note

Funding Information:
We thank Dr. Toshio Imai and National Cancer Center Research Core Facility for preparation of sections in this study. Y.S. is a recipient of Research Resident Fellowships from the Foundation for Promotion of Cancer Research. This work was supported by Grants-in-Aid for the Third-Term Comprehensive Cancer control Strategy from the Ministry of Health, Labor and Welfare, Japan; and by the Global Research Laboratory Program from Korea Foundation for International Cooperation of Science & Technology.

All Science Journal Classification (ASJC) codes

Oncology
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.canlet.2013.07.034

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title = "Interleukin-1β induced by Helicobacter pylori infection enhances mouse gastric carcinogenesis",

abstract = "Interleukin-1β (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 the. Il1b-null mice (58% of WT; P<. 0.005). Mechanistically, HP infection induced NF-κB 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.",

author = "Yasuyuki Shigematsu and Tohru Niwa and Emil Rehnberg and Takeshi Toyoda and Satoshi Yoshida and Akiko Mori and Mika Wakabayashi and Yoichiro Iwakura and Masao Ichinose and Kim, {Yong Joon} and Toshikazu Ushijima",

note = "Funding Information: We thank Dr. Toshio Imai and National Cancer Center Research Core Facility for preparation of sections in this study. Y.S. is a recipient of Research Resident Fellowships from the Foundation for Promotion of Cancer Research. This work was supported by Grants-in-Aid for the Third-Term Comprehensive Cancer control Strategy from the Ministry of Health, Labor and Welfare, Japan; and by the Global Research Laboratory Program from Korea Foundation for International Cooperation of Science & Technology. ",

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doi = "10.1016/j.canlet.2013.07.034",

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AU - Shigematsu, Yasuyuki

AU - Niwa, Tohru

AU - Rehnberg, Emil

AU - Toyoda, Takeshi

AU - Yoshida, Satoshi

AU - Mori, Akiko

AU - Wakabayashi, Mika

AU - Iwakura, Yoichiro

AU - Ichinose, Masao

AU - Kim, Yong Joon

AU - Ushijima, Toshikazu

N1 - Funding Information: We thank Dr. Toshio Imai and National Cancer Center Research Core Facility for preparation of sections in this study. Y.S. is a recipient of Research Resident Fellowships from the Foundation for Promotion of Cancer Research. This work was supported by Grants-in-Aid for the Third-Term Comprehensive Cancer control Strategy from the Ministry of Health, Labor and Welfare, Japan; and by the Global Research Laboratory Program from Korea Foundation for International Cooperation of Science & Technology.

PY - 2013/10/28

Y1 - 2013/10/28

N2 - Interleukin-1β (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 the. Il1b-null mice (58% of WT; P<. 0.005). Mechanistically, HP infection induced NF-κB 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.

AB - Interleukin-1β (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 the. Il1b-null mice (58% of WT; P<. 0.005). Mechanistically, HP infection induced NF-κB 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.

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Interleukin-1β induced by Helicobacter pylori infection enhances mouse gastric carcinogenesis

Abstract

Bibliographical note

All Science Journal Classification (ASJC) codes

UN SDGs

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