The Experts below are selected from a list of 639 Experts worldwide ranked by ideXlab platform

Kanji Tsuchimoto - One of the best experts on this subject based on the ideXlab platform.

  • Microcirculatory alteration in low-grade gastric mucosa-associated lymphoma by Helicobacter Heilmannii infection: its relation to vascular endothelial growth factor and cyclooxygenase-2.
    Journal of gastroenterology and hepatology, 2020
    Co-Authors: Masahiko Nakamura, Somay Yamagata Murayama, Yukie Sekiya, Shinichi Takahashi, Kaori Nishikawa, Tsukasa Matsumoto, Haruki Yamada, Hidenori Matsui, Chihiro Aikawa, Kanji Tsuchimoto
    Abstract:

    There are clinical reports that Helicobacter Heilmannii, as well as Helicobacter pylori, has been clinically reported to cause gastric low-grade mucosa-associated lymphoid tissue-type (MALT) lymphoma, although its precise mechanism remains to be clarified. Thus, the present study was undertaken to elucidate the alteration of the microcirculatory structure and the relation to angiogenetic factors in mice infected with H. Heilmannii for 3 and 6 months. Immunohistochemical studies have been performed by FITC-dextran intra-aortic infusion or CD31, vascular endothelial growth factor-A, cyclooxygenase 2 antibodies using our recently established model of gastric mucosa-associated lymphoid tissue-type gastric B-cell lymphoma in C57BL/6 mice. Increased microcirculatory network was recognized surrounding the MALT lymphoma tissues by both the FITC-dextran infusion method and CD31 immunoreactivity. Vascular endothelial growth factor-A immunoreactivity was recognized within the lymphoma tissues as well as in the marginal area, while cyclooxygenase-2 immunoreactivity was localized in the area surrounding the MALT lymphoma tissues. Increased microvascular network as well as enhanced VEGF-A immunoreactivity was shown to be related to expansion of the MALT lymphoma formed by Helicobacter Heilmannii infection.

  • Short Communication Interaction of VEGF to gastric low grade MALT lymphoma by Helicobacter Heilmannii infection in C57/BL/6 mice
    2020
    Co-Authors: M Nakamura, Tsukasa Matsumoto, Hidenori Matsui, Hirotsugu Yamada, S. Yamagata Murayama, S. Takahashi, Kanji Tsuchimoto
    Abstract:

    Helicobacter Heilmannii (Hh) has been clinically reported to have some relation to gastric low grade MALT lymphoma. Recently, we have formed the gastric MALT lymphoma in C57BL/6 mice. Materials and methods: C57BL/6 mice infected with Hh from cynomolgus monkey for more than 6 months were used. The macroscopic, immunohistochemical and electron microscopic observation was performed Results: MALT lymphoma was formed in almost 100 % of the infected mice. Increased VEGF-A and Flt-3 immunore- activity was recognized. Conclusion: Hh was shown to be related to the formation of MALT lymphoma and VEGF is suggested to play a role in this lymphoma.

  • Suppression of lymphangiogenesis induced by Flt-4 antibody in gastric low-grade mucosa-associated lymphoid tissue lymphoma by Helicobacter Heilmannii infection.
    Journal of gastroenterology and hepatology, 2020
    Co-Authors: Masahiko Nakamura, Shinichi Takahashi, Tetsufumi Takahashi, Hidenori Matsui, Satoshi Ogawa, Ryo Tamura, Somay Y Murayama, Kanji Tsuchimoto
    Abstract:

    Our recent study revealed that per oral infection with Helicobacter Heilmannii induced low-grade mucosa-associated lymphoid tissue (MALT) lymphoma in the gastric fundus of C57BL/6 mice after a period of 6 months, although the pathophysiological mechanism of lymphoma expansion remains to be clarified. The present study was undertaken to elucidate the interaction of this tumor with angiogenesis and lymphangiogenesis. In addition, the effect of Flt-4 antibodies on lymphoma expansion was investigated. C57BL/6 female mice infected with H. Heilmannii for 3 months were used in the experiments. Localization of vascular endothelial growth factor C (VEGF-C) and Flt-4 immunoreactivity were detected by indirect immunohistochemical methods. Localization of lymphatic and vascular endothelial cells was investigated by localization of prox-1. In addition, Flt-4 antibody with and without Flt-1 or Flk-1 antibodies was administered i.p. to clarify their effects on tumor size. MALT lymphoma has a rich microvascular network consisting of immature capillaries, lymphatics and venules. By immunohistochemical analysis, prox-1 immunoreactivity was observed mostly in the marginal area of the lymphoma, where VEGF-C and Flt-4 immunoreactivities were also seen. Stereomicroscopic study revealed that administration of Flt-4 and Flt-1 antibodies significantly reduced the surface area of the lymphoma in the mouse stomach. A VEGF-C-mediated mechanism plays an important role in the expansion of MALT lymphoma and the administration of VEGF receptor antibodies had a suppressive effect on tumor growth.

  • role of substance p and cgrp in gastric malt lymphoma induced by Helicobacter Heilmannii infection 1052 5
    The FASEB Journal, 2014
    Co-Authors: Masahiko Nakamura, Tetsufumi Takahashi, Hidenori Matsui, Kanji Tsuchimoto
    Abstract:

    Recently, many neuroendocrine mediators have been reported to be related to the formation and enlargement of the neoplasm. From our electron microscopic analysis of the gastric MALT lymphoma, many unmyelinated nerve fiber-like structures have been detected especially in the early stage of the tumor formation. Thus, the present study was undertaken to clarify the localization of choline acetyltransferase (ChAc), substance P, its receptor NK-1R, CGRP and RAMP-1, in the MALT lymphoma tissues. The effect of eradication of the bacilli as well as spantide II, a substance P antagonist, was also investigated. Materials and Methods The gastric, hepatic and pulmonary MALT lymphoma was formed by the per oral administration of homogenized gastric mucosa from Helicobacter Heilmannii-infected mice. The localization of ChAc, substance P, NK-1R, CGRP and RAMP-1 was observed by the indirect immunohistochemisty. The eradication treatment was performed by the combined administration of amoxicillin, chlarithromycin and lanso...

  • molecular mechanism of gastric malt lymphoma formation by Helicobacter Heilmannii infection
    Gastroenterology, 2011
    Co-Authors: Tetsufumi Takahashi, Masahiko Nakamura, Shinichi Takahashi, Hidenori Matsui, Asako Takizawa, Yoko Komatsu, Keiko Shinagawa, Toshifumi Hibi, Kanji Tsuchimoto
    Abstract:

    liver. Twelve and eighteen months after the infection, approximately 100% of infected mice had liver and pulmonary lesions. Some of the MALT lymphomas were defined as belonging to the high-grade group by the PCNA positivity. Eradication of the bacteria induced shrinkage of the tumor in the liver and the lung with apoptotic cells as well as in the stomach. Conclusion: Long-term infection with Helicobacter Heilmannii in C57BL/6 mouse induced lowand high-grade hepatic and pulmonary MALT lymphoma as well as gastric lymphoma. Eradication of the bacteria brought about shrinkage of the hepatic and pulmonary lesions as well as gastric MALT lymphoma.

Masahiko Nakamura - One of the best experts on this subject based on the ideXlab platform.

  • Suppression of lymphangiogenesis induced by Flt-4 antibody in gastric low-grade mucosa-associated lymphoid tissue lymphoma by Helicobacter Heilmannii infection.
    Journal of gastroenterology and hepatology, 2020
    Co-Authors: Masahiko Nakamura, Shinichi Takahashi, Tetsufumi Takahashi, Hidenori Matsui, Satoshi Ogawa, Ryo Tamura, Somay Y Murayama, Kanji Tsuchimoto
    Abstract:

    Our recent study revealed that per oral infection with Helicobacter Heilmannii induced low-grade mucosa-associated lymphoid tissue (MALT) lymphoma in the gastric fundus of C57BL/6 mice after a period of 6 months, although the pathophysiological mechanism of lymphoma expansion remains to be clarified. The present study was undertaken to elucidate the interaction of this tumor with angiogenesis and lymphangiogenesis. In addition, the effect of Flt-4 antibodies on lymphoma expansion was investigated. C57BL/6 female mice infected with H. Heilmannii for 3 months were used in the experiments. Localization of vascular endothelial growth factor C (VEGF-C) and Flt-4 immunoreactivity were detected by indirect immunohistochemical methods. Localization of lymphatic and vascular endothelial cells was investigated by localization of prox-1. In addition, Flt-4 antibody with and without Flt-1 or Flk-1 antibodies was administered i.p. to clarify their effects on tumor size. MALT lymphoma has a rich microvascular network consisting of immature capillaries, lymphatics and venules. By immunohistochemical analysis, prox-1 immunoreactivity was observed mostly in the marginal area of the lymphoma, where VEGF-C and Flt-4 immunoreactivities were also seen. Stereomicroscopic study revealed that administration of Flt-4 and Flt-1 antibodies significantly reduced the surface area of the lymphoma in the mouse stomach. A VEGF-C-mediated mechanism plays an important role in the expansion of MALT lymphoma and the administration of VEGF receptor antibodies had a suppressive effect on tumor growth.

  • Microcirculatory alteration in low-grade gastric mucosa-associated lymphoma by Helicobacter Heilmannii infection: its relation to vascular endothelial growth factor and cyclooxygenase-2.
    Journal of gastroenterology and hepatology, 2020
    Co-Authors: Masahiko Nakamura, Somay Yamagata Murayama, Yukie Sekiya, Shinichi Takahashi, Kaori Nishikawa, Tsukasa Matsumoto, Haruki Yamada, Hidenori Matsui, Chihiro Aikawa, Kanji Tsuchimoto
    Abstract:

    There are clinical reports that Helicobacter Heilmannii, as well as Helicobacter pylori, has been clinically reported to cause gastric low-grade mucosa-associated lymphoid tissue-type (MALT) lymphoma, although its precise mechanism remains to be clarified. Thus, the present study was undertaken to elucidate the alteration of the microcirculatory structure and the relation to angiogenetic factors in mice infected with H. Heilmannii for 3 and 6 months. Immunohistochemical studies have been performed by FITC-dextran intra-aortic infusion or CD31, vascular endothelial growth factor-A, cyclooxygenase 2 antibodies using our recently established model of gastric mucosa-associated lymphoid tissue-type gastric B-cell lymphoma in C57BL/6 mice. Increased microcirculatory network was recognized surrounding the MALT lymphoma tissues by both the FITC-dextran infusion method and CD31 immunoreactivity. Vascular endothelial growth factor-A immunoreactivity was recognized within the lymphoma tissues as well as in the marginal area, while cyclooxygenase-2 immunoreactivity was localized in the area surrounding the MALT lymphoma tissues. Increased microvascular network as well as enhanced VEGF-A immunoreactivity was shown to be related to expansion of the MALT lymphoma formed by Helicobacter Heilmannii infection.

  • Alteration of angiogenesis in Helicobacter Heilmannii-induced mucosa-associated lymphoid tissue lymphoma: interaction with c-Met and hepatocyte growth factor.
    Journal of gastroenterology and hepatology, 2020
    Co-Authors: Masahiko Nakamura, Hiroshi Serizawa, Shinichi Takahashi, Tetsufumi Takahashi, Hidenori Matsui, Somay Y Murayama, Yuko Baniwa, Hidekazu Suzuki, Toshifumi Hibi
    Abstract:

    The hepatocyte growth factor (HGF)/c-Met pathway has attracted attention in the formation of malignant tumors, as HGF secreted from the microcirculatory components as well as residing macrophages has been suggested to act on the c-Met receptors of cancer cells to decrease apoptosis and increase proliferation, invasion, and metastasis. The present study was undertaken to elucidate the interaction of the gastric, hepatic, and pulmonary mucosa-associated lymphoid tissue (MALT) lymphoma induced by Helicobacter Heilmannii infection with c-Met and HGF. C57BL/6 female mice, infected with H. Heilmannii for 3 months were used. The localization of the HGF, c-Met, and HGF activator immunoreactivities was observed by the indirect immunohistochemical methods. In addition, the effect of c-Met antibody and c-Met inhibitor, PHA-665752, was also investigated. c-Met immunoreactivity was found in the lymphocytes composing the MALT lymphoma, and HGF immunoreactivity was recognized mostly in the endothelial cells and macrophages in the MALT lymphoma. HGFA was localized on mesenchymal cells other than the lymphocytes. The administration of the antibody against c-Met or the c-Met inhibitor to the infected mice induced the significant suppression of hepatic and pulmonary MALT lymphoma, while the gastric MALT lymphoma showed only a tendency to decrease in size, while the active caspase 3 positive cells markedly decreased in the gastric, hepatic, and pulmonary MALT lymphoma after the treatment with the c-Met antibody or the c-Met antagonist. HGF and c-Met pathway were suggested to contribute to the lymphomagenesis in the MALT lymphoma after H. Heilmannii infection. © 2014 Journal of Gastroenterology and Hepatology Foundation and Wiley Publishing Asia Pty Ltd.

  • Helicobacter suis infected nodular gastritis and a review of diagnostic sensitivity for Helicobacter Heilmannii like organisms
    Case Reports in Gastroenterology, 2015
    Co-Authors: Shigeki Goji, Masahiko Nakamura, Somay Yamagata Murayama, Hidenori Matsui, Yasuhiro Tamura, Makoto Sasaki, Naotaka Ogasawara, Yasushi Funaki, Kunio Kasugai
    Abstract:

    Helicobacter Heilmannii -like organisms (HHLOs) are associated with mucosa-associated lymphoid tissue lymphoma and peptic ulcer. However, the sensitivity of diagnostic tests for HHLO

  • alteration of angiogenesis in Helicobacter Heilmannii induced mucosa associated lymphoid tissue lymphoma interaction with c met and hepatocyte growth factor
    Journal of Gastroenterology and Hepatology, 2014
    Co-Authors: Masahiko Nakamura, Somay Yamagata Murayama, Hiroshi Serizawa, Shinichi Takahashi, Tetsufumi Takahashi, Hidenori Matsui, Yuko Baniwa, Hidekazu Suzuki, Toshifumi Hibi
    Abstract:

    Background and Aim The hepatocyte growth factor (HGF)/c-Met pathway has attracted attention in the formation of malignant tumors, as HGF secreted from the microcirculatory components as well as residing macrophages has been suggested to act on the c-Met receptors of cancer cells to decrease apoptosis and increase proliferation, invasion, and metastasis. The present study was undertaken to elucidate the interaction of the gastric, hepatic, and pulmonary mucosa-associated lymphoid tissue (MALT) lymphoma induced by Helicobacter Heilmannii infection with c-Met and HGF. Methods C57BL/6 female mice, infected with H. Heilmannii for 3 months were used. The localization of the HGF, c-Met, and HGF activator immunoreactivities was observed by the indirect immunohistochemical methods. In addition, the effect of c-Met antibody and c-Met inhibitor, PHA-665752, was also investigated. Results c-Met immunoreactivity was found in the lymphocytes composing the MALT lymphoma, and HGF immunoreactivity was recognized mostly in the endothelial cells and macrophages in the MALT lymphoma. HGFA was localized on mesenchymal cells other than the lymphocytes. The administration of the antibody against c-Met or the c-Met inhibitor to the infected mice induced the significant suppression of hepatic and pulmonary MALT lymphoma, while the gastric MALT lymphoma showed only a tendency to decrease in size, while the active caspase 3 positive cells markedly decreased in the gastric, hepatic, and pulmonary MALT lymphoma after the treatment with the c-Met antibody or the c-Met antagonist. Conclusions HGF and c-Met pathway were suggested to contribute to the lymphomagenesis in the MALT lymphoma after H. Heilmannii infection.

Hidenori Matsui - One of the best experts on this subject based on the ideXlab platform.

  • Short Communication Interaction of VEGF to gastric low grade MALT lymphoma by Helicobacter Heilmannii infection in C57/BL/6 mice
    2020
    Co-Authors: M Nakamura, Tsukasa Matsumoto, Hidenori Matsui, Hirotsugu Yamada, S. Yamagata Murayama, S. Takahashi, Kanji Tsuchimoto
    Abstract:

    Helicobacter Heilmannii (Hh) has been clinically reported to have some relation to gastric low grade MALT lymphoma. Recently, we have formed the gastric MALT lymphoma in C57BL/6 mice. Materials and methods: C57BL/6 mice infected with Hh from cynomolgus monkey for more than 6 months were used. The macroscopic, immunohistochemical and electron microscopic observation was performed Results: MALT lymphoma was formed in almost 100 % of the infected mice. Increased VEGF-A and Flt-3 immunore- activity was recognized. Conclusion: Hh was shown to be related to the formation of MALT lymphoma and VEGF is suggested to play a role in this lymphoma.

  • Alteration of angiogenesis in Helicobacter Heilmannii-induced mucosa-associated lymphoid tissue lymphoma: interaction with c-Met and hepatocyte growth factor.
    Journal of gastroenterology and hepatology, 2020
    Co-Authors: Masahiko Nakamura, Hiroshi Serizawa, Shinichi Takahashi, Tetsufumi Takahashi, Hidenori Matsui, Somay Y Murayama, Yuko Baniwa, Hidekazu Suzuki, Toshifumi Hibi
    Abstract:

    The hepatocyte growth factor (HGF)/c-Met pathway has attracted attention in the formation of malignant tumors, as HGF secreted from the microcirculatory components as well as residing macrophages has been suggested to act on the c-Met receptors of cancer cells to decrease apoptosis and increase proliferation, invasion, and metastasis. The present study was undertaken to elucidate the interaction of the gastric, hepatic, and pulmonary mucosa-associated lymphoid tissue (MALT) lymphoma induced by Helicobacter Heilmannii infection with c-Met and HGF. C57BL/6 female mice, infected with H. Heilmannii for 3 months were used. The localization of the HGF, c-Met, and HGF activator immunoreactivities was observed by the indirect immunohistochemical methods. In addition, the effect of c-Met antibody and c-Met inhibitor, PHA-665752, was also investigated. c-Met immunoreactivity was found in the lymphocytes composing the MALT lymphoma, and HGF immunoreactivity was recognized mostly in the endothelial cells and macrophages in the MALT lymphoma. HGFA was localized on mesenchymal cells other than the lymphocytes. The administration of the antibody against c-Met or the c-Met inhibitor to the infected mice induced the significant suppression of hepatic and pulmonary MALT lymphoma, while the gastric MALT lymphoma showed only a tendency to decrease in size, while the active caspase 3 positive cells markedly decreased in the gastric, hepatic, and pulmonary MALT lymphoma after the treatment with the c-Met antibody or the c-Met antagonist. HGF and c-Met pathway were suggested to contribute to the lymphomagenesis in the MALT lymphoma after H. Heilmannii infection. © 2014 Journal of Gastroenterology and Hepatology Foundation and Wiley Publishing Asia Pty Ltd.

  • Suppression of lymphangiogenesis induced by Flt-4 antibody in gastric low-grade mucosa-associated lymphoid tissue lymphoma by Helicobacter Heilmannii infection.
    Journal of gastroenterology and hepatology, 2020
    Co-Authors: Masahiko Nakamura, Shinichi Takahashi, Tetsufumi Takahashi, Hidenori Matsui, Satoshi Ogawa, Ryo Tamura, Somay Y Murayama, Kanji Tsuchimoto
    Abstract:

    Our recent study revealed that per oral infection with Helicobacter Heilmannii induced low-grade mucosa-associated lymphoid tissue (MALT) lymphoma in the gastric fundus of C57BL/6 mice after a period of 6 months, although the pathophysiological mechanism of lymphoma expansion remains to be clarified. The present study was undertaken to elucidate the interaction of this tumor with angiogenesis and lymphangiogenesis. In addition, the effect of Flt-4 antibodies on lymphoma expansion was investigated. C57BL/6 female mice infected with H. Heilmannii for 3 months were used in the experiments. Localization of vascular endothelial growth factor C (VEGF-C) and Flt-4 immunoreactivity were detected by indirect immunohistochemical methods. Localization of lymphatic and vascular endothelial cells was investigated by localization of prox-1. In addition, Flt-4 antibody with and without Flt-1 or Flk-1 antibodies was administered i.p. to clarify their effects on tumor size. MALT lymphoma has a rich microvascular network consisting of immature capillaries, lymphatics and venules. By immunohistochemical analysis, prox-1 immunoreactivity was observed mostly in the marginal area of the lymphoma, where VEGF-C and Flt-4 immunoreactivities were also seen. Stereomicroscopic study revealed that administration of Flt-4 and Flt-1 antibodies significantly reduced the surface area of the lymphoma in the mouse stomach. A VEGF-C-mediated mechanism plays an important role in the expansion of MALT lymphoma and the administration of VEGF receptor antibodies had a suppressive effect on tumor growth.

  • Microcirculatory alteration in low-grade gastric mucosa-associated lymphoma by Helicobacter Heilmannii infection: its relation to vascular endothelial growth factor and cyclooxygenase-2.
    Journal of gastroenterology and hepatology, 2020
    Co-Authors: Masahiko Nakamura, Somay Yamagata Murayama, Yukie Sekiya, Shinichi Takahashi, Kaori Nishikawa, Tsukasa Matsumoto, Haruki Yamada, Hidenori Matsui, Chihiro Aikawa, Kanji Tsuchimoto
    Abstract:

    There are clinical reports that Helicobacter Heilmannii, as well as Helicobacter pylori, has been clinically reported to cause gastric low-grade mucosa-associated lymphoid tissue-type (MALT) lymphoma, although its precise mechanism remains to be clarified. Thus, the present study was undertaken to elucidate the alteration of the microcirculatory structure and the relation to angiogenetic factors in mice infected with H. Heilmannii for 3 and 6 months. Immunohistochemical studies have been performed by FITC-dextran intra-aortic infusion or CD31, vascular endothelial growth factor-A, cyclooxygenase 2 antibodies using our recently established model of gastric mucosa-associated lymphoid tissue-type gastric B-cell lymphoma in C57BL/6 mice. Increased microcirculatory network was recognized surrounding the MALT lymphoma tissues by both the FITC-dextran infusion method and CD31 immunoreactivity. Vascular endothelial growth factor-A immunoreactivity was recognized within the lymphoma tissues as well as in the marginal area, while cyclooxygenase-2 immunoreactivity was localized in the area surrounding the MALT lymphoma tissues. Increased microvascular network as well as enhanced VEGF-A immunoreactivity was shown to be related to expansion of the MALT lymphoma formed by Helicobacter Heilmannii infection.

  • Helicobacter suis infected nodular gastritis and a review of diagnostic sensitivity for Helicobacter Heilmannii like organisms
    Case Reports in Gastroenterology, 2015
    Co-Authors: Shigeki Goji, Masahiko Nakamura, Somay Yamagata Murayama, Hidenori Matsui, Yasuhiro Tamura, Makoto Sasaki, Naotaka Ogasawara, Yasushi Funaki, Kunio Kasugai
    Abstract:

    Helicobacter Heilmannii -like organisms (HHLOs) are associated with mucosa-associated lymphoid tissue lymphoma and peptic ulcer. However, the sensitivity of diagnostic tests for HHLO

Shinichi Takahashi - One of the best experts on this subject based on the ideXlab platform.

  • Suppression of lymphangiogenesis induced by Flt-4 antibody in gastric low-grade mucosa-associated lymphoid tissue lymphoma by Helicobacter Heilmannii infection.
    Journal of gastroenterology and hepatology, 2020
    Co-Authors: Masahiko Nakamura, Shinichi Takahashi, Tetsufumi Takahashi, Hidenori Matsui, Satoshi Ogawa, Ryo Tamura, Somay Y Murayama, Kanji Tsuchimoto
    Abstract:

    Our recent study revealed that per oral infection with Helicobacter Heilmannii induced low-grade mucosa-associated lymphoid tissue (MALT) lymphoma in the gastric fundus of C57BL/6 mice after a period of 6 months, although the pathophysiological mechanism of lymphoma expansion remains to be clarified. The present study was undertaken to elucidate the interaction of this tumor with angiogenesis and lymphangiogenesis. In addition, the effect of Flt-4 antibodies on lymphoma expansion was investigated. C57BL/6 female mice infected with H. Heilmannii for 3 months were used in the experiments. Localization of vascular endothelial growth factor C (VEGF-C) and Flt-4 immunoreactivity were detected by indirect immunohistochemical methods. Localization of lymphatic and vascular endothelial cells was investigated by localization of prox-1. In addition, Flt-4 antibody with and without Flt-1 or Flk-1 antibodies was administered i.p. to clarify their effects on tumor size. MALT lymphoma has a rich microvascular network consisting of immature capillaries, lymphatics and venules. By immunohistochemical analysis, prox-1 immunoreactivity was observed mostly in the marginal area of the lymphoma, where VEGF-C and Flt-4 immunoreactivities were also seen. Stereomicroscopic study revealed that administration of Flt-4 and Flt-1 antibodies significantly reduced the surface area of the lymphoma in the mouse stomach. A VEGF-C-mediated mechanism plays an important role in the expansion of MALT lymphoma and the administration of VEGF receptor antibodies had a suppressive effect on tumor growth.

  • Microcirculatory alteration in low-grade gastric mucosa-associated lymphoma by Helicobacter Heilmannii infection: its relation to vascular endothelial growth factor and cyclooxygenase-2.
    Journal of gastroenterology and hepatology, 2020
    Co-Authors: Masahiko Nakamura, Somay Yamagata Murayama, Yukie Sekiya, Shinichi Takahashi, Kaori Nishikawa, Tsukasa Matsumoto, Haruki Yamada, Hidenori Matsui, Chihiro Aikawa, Kanji Tsuchimoto
    Abstract:

    There are clinical reports that Helicobacter Heilmannii, as well as Helicobacter pylori, has been clinically reported to cause gastric low-grade mucosa-associated lymphoid tissue-type (MALT) lymphoma, although its precise mechanism remains to be clarified. Thus, the present study was undertaken to elucidate the alteration of the microcirculatory structure and the relation to angiogenetic factors in mice infected with H. Heilmannii for 3 and 6 months. Immunohistochemical studies have been performed by FITC-dextran intra-aortic infusion or CD31, vascular endothelial growth factor-A, cyclooxygenase 2 antibodies using our recently established model of gastric mucosa-associated lymphoid tissue-type gastric B-cell lymphoma in C57BL/6 mice. Increased microcirculatory network was recognized surrounding the MALT lymphoma tissues by both the FITC-dextran infusion method and CD31 immunoreactivity. Vascular endothelial growth factor-A immunoreactivity was recognized within the lymphoma tissues as well as in the marginal area, while cyclooxygenase-2 immunoreactivity was localized in the area surrounding the MALT lymphoma tissues. Increased microvascular network as well as enhanced VEGF-A immunoreactivity was shown to be related to expansion of the MALT lymphoma formed by Helicobacter Heilmannii infection.

  • Alteration of angiogenesis in Helicobacter Heilmannii-induced mucosa-associated lymphoid tissue lymphoma: interaction with c-Met and hepatocyte growth factor.
    Journal of gastroenterology and hepatology, 2020
    Co-Authors: Masahiko Nakamura, Hiroshi Serizawa, Shinichi Takahashi, Tetsufumi Takahashi, Hidenori Matsui, Somay Y Murayama, Yuko Baniwa, Hidekazu Suzuki, Toshifumi Hibi
    Abstract:

    The hepatocyte growth factor (HGF)/c-Met pathway has attracted attention in the formation of malignant tumors, as HGF secreted from the microcirculatory components as well as residing macrophages has been suggested to act on the c-Met receptors of cancer cells to decrease apoptosis and increase proliferation, invasion, and metastasis. The present study was undertaken to elucidate the interaction of the gastric, hepatic, and pulmonary mucosa-associated lymphoid tissue (MALT) lymphoma induced by Helicobacter Heilmannii infection with c-Met and HGF. C57BL/6 female mice, infected with H. Heilmannii for 3 months were used. The localization of the HGF, c-Met, and HGF activator immunoreactivities was observed by the indirect immunohistochemical methods. In addition, the effect of c-Met antibody and c-Met inhibitor, PHA-665752, was also investigated. c-Met immunoreactivity was found in the lymphocytes composing the MALT lymphoma, and HGF immunoreactivity was recognized mostly in the endothelial cells and macrophages in the MALT lymphoma. HGFA was localized on mesenchymal cells other than the lymphocytes. The administration of the antibody against c-Met or the c-Met inhibitor to the infected mice induced the significant suppression of hepatic and pulmonary MALT lymphoma, while the gastric MALT lymphoma showed only a tendency to decrease in size, while the active caspase 3 positive cells markedly decreased in the gastric, hepatic, and pulmonary MALT lymphoma after the treatment with the c-Met antibody or the c-Met antagonist. HGF and c-Met pathway were suggested to contribute to the lymphomagenesis in the MALT lymphoma after H. Heilmannii infection. © 2014 Journal of Gastroenterology and Hepatology Foundation and Wiley Publishing Asia Pty Ltd.

  • alteration of angiogenesis in Helicobacter Heilmannii induced mucosa associated lymphoid tissue lymphoma interaction with c met and hepatocyte growth factor
    Journal of Gastroenterology and Hepatology, 2014
    Co-Authors: Masahiko Nakamura, Somay Yamagata Murayama, Hiroshi Serizawa, Shinichi Takahashi, Tetsufumi Takahashi, Hidenori Matsui, Yuko Baniwa, Hidekazu Suzuki, Toshifumi Hibi
    Abstract:

    Background and Aim The hepatocyte growth factor (HGF)/c-Met pathway has attracted attention in the formation of malignant tumors, as HGF secreted from the microcirculatory components as well as residing macrophages has been suggested to act on the c-Met receptors of cancer cells to decrease apoptosis and increase proliferation, invasion, and metastasis. The present study was undertaken to elucidate the interaction of the gastric, hepatic, and pulmonary mucosa-associated lymphoid tissue (MALT) lymphoma induced by Helicobacter Heilmannii infection with c-Met and HGF. Methods C57BL/6 female mice, infected with H. Heilmannii for 3 months were used. The localization of the HGF, c-Met, and HGF activator immunoreactivities was observed by the indirect immunohistochemical methods. In addition, the effect of c-Met antibody and c-Met inhibitor, PHA-665752, was also investigated. Results c-Met immunoreactivity was found in the lymphocytes composing the MALT lymphoma, and HGF immunoreactivity was recognized mostly in the endothelial cells and macrophages in the MALT lymphoma. HGFA was localized on mesenchymal cells other than the lymphocytes. The administration of the antibody against c-Met or the c-Met inhibitor to the infected mice induced the significant suppression of hepatic and pulmonary MALT lymphoma, while the gastric MALT lymphoma showed only a tendency to decrease in size, while the active caspase 3 positive cells markedly decreased in the gastric, hepatic, and pulmonary MALT lymphoma after the treatment with the c-Met antibody or the c-Met antagonist. Conclusions HGF and c-Met pathway were suggested to contribute to the lymphomagenesis in the MALT lymphoma after H. Heilmannii infection.

  • molecular mechanism of gastric malt lymphoma formation by Helicobacter Heilmannii infection
    Gastroenterology, 2011
    Co-Authors: Tetsufumi Takahashi, Masahiko Nakamura, Shinichi Takahashi, Hidenori Matsui, Asako Takizawa, Yoko Komatsu, Keiko Shinagawa, Toshifumi Hibi, Kanji Tsuchimoto
    Abstract:

    liver. Twelve and eighteen months after the infection, approximately 100% of infected mice had liver and pulmonary lesions. Some of the MALT lymphomas were defined as belonging to the high-grade group by the PCNA positivity. Eradication of the bacteria induced shrinkage of the tumor in the liver and the lung with apoptotic cells as well as in the stomach. Conclusion: Long-term infection with Helicobacter Heilmannii in C57BL/6 mouse induced lowand high-grade hepatic and pulmonary MALT lymphoma as well as gastric lymphoma. Eradication of the bacteria brought about shrinkage of the hepatic and pulmonary lesions as well as gastric MALT lymphoma.

Freddy Haesebrouck - One of the best experts on this subject based on the ideXlab platform.

  • Peptic ulcer disease associated with Helicobacter felis in a dog owner
    European Journal of Gastroenterology & Hepatology, 2020
    Co-Authors: Manuelle De Bock, Kathleen Van Den Bulck, Jean-claude Debongnie, Freddy Haesebrouck, Ann Hellemans, Sylvie Daminet, Jean-charles Coche, Annemie Decostere, Richard Ducatelle
    Abstract:

    The aim of this study was to investigate the identity of the Helicobacter Heilmannii-like bacteria found in the stomach of a human patient suffering from stomach ulcers and her asymptomatic pet dog. An elderly woman was referred for gastroscopy because of right hypochondrial pain, nausea, anorexia a

  • Prevalence of Coinfection with Gastric Non-Helicobacter pylori Helicobacter (NHPH) Species in Helicobacter pylori-infected Patients Suffering from Gastric Disease in Beijing, China.
    Helicobacter, 2014
    Co-Authors: Lihua He, Bram Flahou, Freddy Haesebrouck, Yanan Gong, Jianzhong Zhang
    Abstract:

    Background: The Helicobacter Heilmannii sensu lato (H. Heilmannii s.l.) group consists of long, spiral-shaped bacteria naturally colonizing the stomach of animals. Moreover, bacteria belonging to this group have been observed in 0.2–6% of human gastric biopsy specimens, and associations have been made with the development of chronic gastritis, peptic ulceration, and gastric MALT lymphoma in humans. Materials and Methods: To gain insight into the prevalence of H. Heilmannii s.l. infections in patients suffering from gastric disease in China, H. Heilmannii s.l. species-specific PCRs were performed on DNA extracts from rapid urease test (RUT)-positive gastric biopsies from 1517 patients followed by nucleotide sequencing. At the same time, Helicobacter pylori cultivation and specific PCR was performed to assess H. pylori infection in these patients. Results: In total, H. Heilmannii s.l. infection was detected in 11.87% (178/1499) of H. pylori-positive patients. The prevalence of H. suis, H. felis, H. bizzozeronii, H. Heilmannii sensu stricto (s.s.), and H. salomonis in the patients was 6.94%, 2.20%, 0.13%, 0.07%, and 2.54%, respectively. Results revealed that all patients with H. Heilmannii s.l. infection were co-infected with H. pylori ,a nd some patients were co-infected with more than two different Helicobacter species. Conclusions: Helicobacter Heilmannii s.l. infections are fairly common in Chinese patients. This should be kept in mind when diagnosing the cause of gastric pathologies in patients. Helicobacter suis was shown to be by far the most prevalent H. Heilmannii s.l.species.

  • gastric de novo muc13 expression and spasmolytic polypeptide expressing metaplasia during Helicobacter Heilmannii infection
    Infection and Immunity, 2014
    Co-Authors: Annemieke Smet, Bram Flahou, Richard Ducatelle, Caroline Blaecher, Sara K Linden, Freddy Haesebrouck
    Abstract:

    Helicobacter Heilmannii is a zoonotic bacterium that has been associated with gastric disease in humans. In this study, the mRNA expression of mucins in the stomach of BALB/c mice was analyzed at several time points during a 1-year infection with this bacterium, during which gastric disease progressed in severity. Markers for acid production by parietal cells and mucous metaplasia were also examined. In the first 9 weeks postinfection, the mRNA expression of Muc6 was clearly upregulated in both the antrum and fundus of the stomach of H. Heilmannii-infected mice. Interestingly, Muc13 was upregulated already at 1 day postinfection in the fundus of the stomach. Its expression level remained high in the stomach over the course of the infection. This mucin is, however, not expressed in a healthy stomach, and high expression of this mucin has so far only been described in gastric cancer. In the later stages of infection, mRNA expression of H+/K+-ATPase alpha/beta and KCNQ1 decreased, whereas the expression of Muc4, Tff2, Dmbt1, and polymeric immunoglobulin receptor (pIgR) increased starting at 16 weeks postinfection onwards, suggesting the existence of spasmolytic polypeptide-expressing metaplasia in the fundus of the stomach. Mucous metaplasia present in the mucosa surrounding low-grade mucosa-associated lymphoid tissue (MALT) lymphoma-like lesions was also histologically confirmed. Our findings indicate that H. Heilmannii infection causes severe gastric pathologies and alterations in the expression pattern of gastric mucins, such as Muc6 and Muc13, as well as disrupting gastric homeostasis by inducing the loss of parietal cells, resulting in the development of mucous metaplasia.

  • genome sequence of Helicobacter Heilmannii sensu stricto asb1 isolated from the gastric mucosa of a kitten with severe gastritis
    Genome Announcements, 2013
    Co-Authors: Annemieke Smet, Bram Flahou, Richard Ducatelle, Filip Van Nieuwerburgh, Jessica Ledesma, Dieter Deforce, Freddy Haesebrouck
    Abstract:

    ABSTRACT Here we report the genome sequence of Helicobacter Heilmannii sensu stricto ASB1 isolated from the gastric mucosa of a kitten with severe gastritis. Helicobacter Heilmannii sensu stricto has also been associated with gastric disease in humans. Availability of this genome sequence will contribute to the identification of genes involved in the pathogen9s virulence and carcinogenic properties.

  • Helicobacter Heilmannii sp nov isolated from feline gastric mucosa
    International Journal of Systematic and Evolutionary Microbiology, 2012
    Co-Authors: Annemieke Smet, Bram Flahou, Peter Vandamme, Frank Pasmans, Richard Ducatelle, Katharina Dherde, Ilse Cleenwerck, Freddy Haesebrouck
    Abstract:

    Three Gram-negative, microaerophilic bacteria, strains ASB1T, ASB2 and ASB3, with a corkscrew-like morphology isolated from the gastric mucosa of cats were studied using a polyphasic taxonomic approach. The isolates grew on biphasic culture plates under microaerobic conditions at 37 °C and exhibited urease, oxidase and catalase activities. They were also able to grow in colonies on dry agar plates. Based on 16S rRNA gene sequence analysis, ASB1T, ASB2 and ASB3 were identified as members of the genus Helicobacter and showed 98 to 99 % sequence similarity to strains of Helicobacter felis, Helicobacter bizzozeronii, ‘Candidatus Helicobacter Heilmannii’, Helicobacter cynogastricus, Helicobacter baculiformis and Helicobacter salomonis, six related Helicobacter species previously detected in feline or canine gastric mucosa. Sequencing of the partial hsp60 gene demonstrated that ASB1T, ASB2 and ASB3 constitute a separate taxon among the feline and canine Helicobacter species. The urease gene sequences of ASB1T, ASB2 and ASB3 showed approximately 91 % similarity to those of ‘Candidatus Helicobacter Heilmannii’. Protein profiling, the absence of alkaline phosphatase activity and several other biochemical characteristics also allowed strains ASB1T, ASB2 and ASB3 to be differentiated from other Helicobacter species of feline or canine gastric origin. The results of this polyphasic taxonomic study show that the cultured isolates constitute a new taxon corresponding to ‘Candidatus Helicobacter Heilmannii’, which was previously demonstrated in the stomach of humans, wild felidae, cats and dogs. The name Helicobacter Heilmannii sp. nov. is proposed for these isolates; the type strain is ASB1T ( = DSM 23983T = LMG 26292T).