Interferon-γ regulates apoptosis by releasing soluble tumor necrosis factor receptors in a gastric epithelial cell line

Shimako Furuta, Hidemi Goto, Yasumasa Niwa, Naoki Ohmiya, Kenji Kamiya, Akihiko Oguri, Tetsuo Hayakawa, Naoyoshi Mori

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Background and Aims: Interferon (IFN)-γ and tumor necrosis factor (TNF) are predominant cytokines produced in the gastric mucosa of patients with Helicobacter pylori-infected gastritis. Several studies reported that IFN-γ and TNF induced the synergistic effect on many cell lines. We attempted to clarify the apoptotic activity and the synergistic effect of IFN-γ and TNF on the gastric epithelial cell, and whether IFN-γ relates to soluble TNF receptors (sTNF-R) release from the gastric epithelial cell. Methods: On the gastric epithelial cell line MKN45, cytotoxic and apoptotic effects of IFN-γ and TNF were examined. Next, sTNF-R released in response to IFN-γ and the protective effect of sTNF-R against the cytotoxic activity of TNF and IFN-γ were examined by blocking the release of sTNF-R with a serine protease inhibitor such as phenylmethylsulfonyl fluoride. Results: Interferon-γ significantly decreased cell viability, but TNF decreased it only slightly. Interferon-γ and TNF did not make a synergistic effect on cell viability and apoptosis. Interferon-γ and TNF induced sTNF-R release from gastric epithelial cells. Phenylmethylsulfonyl fluoride significantly inhibited shedding of sTNF-R and a synergistic effect of TNF and IFN-γ on apoptosis was observed. Conclusion: These results suggest that sTNF-R released by IFN-γ regulate the injury on the gastric epithelial cell line induced by TNF.

Original languageEnglish
Pages (from-to)1283-1290
Number of pages8
JournalJournal of Gastroenterology and Hepatology (Australia)
Volume17
Issue number12
DOIs
Publication statusPublished - 01-01-2002

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Tumor Necrosis Factor Receptors
Interferons
Stomach
Epithelial Cells
Apoptosis
Tumor Necrosis Factor-alpha
Cell Line
Phenylmethylsulfonyl Fluoride
Cell Survival
Serine Proteinase Inhibitors
Gastritis
Gastric Mucosa
Helicobacter pylori
Cytokines

All Science Journal Classification (ASJC) codes

  • Hepatology
  • Gastroenterology

Cite this

Furuta, Shimako ; Goto, Hidemi ; Niwa, Yasumasa ; Ohmiya, Naoki ; Kamiya, Kenji ; Oguri, Akihiko ; Hayakawa, Tetsuo ; Mori, Naoyoshi. / Interferon-γ regulates apoptosis by releasing soluble tumor necrosis factor receptors in a gastric epithelial cell line. In: Journal of Gastroenterology and Hepatology (Australia). 2002 ; Vol. 17, No. 12. pp. 1283-1290.
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Interferon-γ regulates apoptosis by releasing soluble tumor necrosis factor receptors in a gastric epithelial cell line. / Furuta, Shimako; Goto, Hidemi; Niwa, Yasumasa; Ohmiya, Naoki; Kamiya, Kenji; Oguri, Akihiko; Hayakawa, Tetsuo; Mori, Naoyoshi.

In: Journal of Gastroenterology and Hepatology (Australia), Vol. 17, No. 12, 01.01.2002, p. 1283-1290.

Research output: Contribution to journalArticle

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T1 - Interferon-γ regulates apoptosis by releasing soluble tumor necrosis factor receptors in a gastric epithelial cell line

AU - Furuta, Shimako

AU - Goto, Hidemi

AU - Niwa, Yasumasa

AU - Ohmiya, Naoki

AU - Kamiya, Kenji

AU - Oguri, Akihiko

AU - Hayakawa, Tetsuo

AU - Mori, Naoyoshi

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N2 - Background and Aims: Interferon (IFN)-γ and tumor necrosis factor (TNF) are predominant cytokines produced in the gastric mucosa of patients with Helicobacter pylori-infected gastritis. Several studies reported that IFN-γ and TNF induced the synergistic effect on many cell lines. We attempted to clarify the apoptotic activity and the synergistic effect of IFN-γ and TNF on the gastric epithelial cell, and whether IFN-γ relates to soluble TNF receptors (sTNF-R) release from the gastric epithelial cell. Methods: On the gastric epithelial cell line MKN45, cytotoxic and apoptotic effects of IFN-γ and TNF were examined. Next, sTNF-R released in response to IFN-γ and the protective effect of sTNF-R against the cytotoxic activity of TNF and IFN-γ were examined by blocking the release of sTNF-R with a serine protease inhibitor such as phenylmethylsulfonyl fluoride. Results: Interferon-γ significantly decreased cell viability, but TNF decreased it only slightly. Interferon-γ and TNF did not make a synergistic effect on cell viability and apoptosis. Interferon-γ and TNF induced sTNF-R release from gastric epithelial cells. Phenylmethylsulfonyl fluoride significantly inhibited shedding of sTNF-R and a synergistic effect of TNF and IFN-γ on apoptosis was observed. Conclusion: These results suggest that sTNF-R released by IFN-γ regulate the injury on the gastric epithelial cell line induced by TNF.

AB - Background and Aims: Interferon (IFN)-γ and tumor necrosis factor (TNF) are predominant cytokines produced in the gastric mucosa of patients with Helicobacter pylori-infected gastritis. Several studies reported that IFN-γ and TNF induced the synergistic effect on many cell lines. We attempted to clarify the apoptotic activity and the synergistic effect of IFN-γ and TNF on the gastric epithelial cell, and whether IFN-γ relates to soluble TNF receptors (sTNF-R) release from the gastric epithelial cell. Methods: On the gastric epithelial cell line MKN45, cytotoxic and apoptotic effects of IFN-γ and TNF were examined. Next, sTNF-R released in response to IFN-γ and the protective effect of sTNF-R against the cytotoxic activity of TNF and IFN-γ were examined by blocking the release of sTNF-R with a serine protease inhibitor such as phenylmethylsulfonyl fluoride. Results: Interferon-γ significantly decreased cell viability, but TNF decreased it only slightly. Interferon-γ and TNF did not make a synergistic effect on cell viability and apoptosis. Interferon-γ and TNF induced sTNF-R release from gastric epithelial cells. Phenylmethylsulfonyl fluoride significantly inhibited shedding of sTNF-R and a synergistic effect of TNF and IFN-γ on apoptosis was observed. Conclusion: These results suggest that sTNF-R released by IFN-γ regulate the injury on the gastric epithelial cell line induced by TNF.

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