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Essential Roles of IL-6 Trans-Signaling in Colonic Epithelial Cells, Induced by the IL-6/Soluble-IL-6 Receptor Derived from Lamina Propria Macrophages, on the Development of Colitis-Associated Premalignant Cancer in a Murine Model

Matsumoto, Satoshi ; Hara, Taeko ; Mitsuyama, Keiichi ; Yamamoto, Mayuko ; Tsuruta, Osamu ; Sata, Michio ; Scheller, Jurgen ; Rose-John, Stefan ; Kado, Sho-ichi ; Takada, Toshihiko

The Journal of immunology (1950), 2010-02, Vol.184 (3), p.1543-1551 [Periódico revisado por pares]

United States: Am Assoc Immnol

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Título:
Essential Roles of IL-6 Trans-Signaling in Colonic Epithelial Cells, Induced by the IL-6/Soluble-IL-6 Receptor Derived from Lamina Propria Macrophages, on the Development of Colitis-Associated Premalignant Cancer in a Murine Model
Autor: Matsumoto, Satoshi ; Hara, Taeko ; Mitsuyama, Keiichi ; Yamamoto, Mayuko ; Tsuruta, Osamu ; Sata, Michio ; Scheller, Jurgen ; Rose-John, Stefan ; Kado, Sho-ichi ; Takada, Toshihiko
Assuntos: Animals ; Chronic Disease ; Colon - cytology ; Colon - immunology ; Colorectal Neoplasms - immunology ; Colorectal Neoplasms - pathology ; Dextran Sulfate - administration & dosage ; Disease Models, Animal ; Female ; Inflammation Mediators - administration & dosage ; Interleukin-6 - physiology ; Intestinal Mucosa - immunology ; Intestinal Mucosa - pathology ; Macrophages - immunology ; Macrophages - metabolism ; Macrophages - pathology ; Mice ; Mice, Inbred BALB C ; Mucous Membrane - immunology ; Mucous Membrane - pathology ; Precancerous Conditions - immunology ; Precancerous Conditions - pathology ; Receptors, Interleukin-6 - physiology ; Signal Transduction - immunology
É parte de: The Journal of immunology (1950), 2010-02, Vol.184 (3), p.1543-1551
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
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Descrição: Activation of the IL-6/Stat3 via IL-6 trans-signaling plays an important role in the pathogenesis of inflammatory bowel disease. Colitis-associated cancer (CAC) is a large bowel cancer and occurs with long-standing inflammatory bowel disease. The role of the IL-6/Stat3 in the development of CAC has not been fully understood. We investigate whether IL-6 trans-signaling contributes to the development of CAC using a mouse colitis-associated premalignant cancer (CApC) model. Chronic colitis (CC) was induced in BALB/c mice using dextran sodium sulfate. CApC was induced by dextran sodium sulfate treatment to CC-affected mice. IL-6 expression was determined by quantitative RT-PCR and immunofluorescence staining in colon. Phospho-Stat3 expression was examined by Western blotting and immunofluorescence analysis. The expression of IL-6 receptors (i.e., the IL-6R alpha-chain and gp130) and tumor necrosis factor-alpha converting enzyme in the colon was examined by laser-capture microdissection and immunofluorescence staining. Soluble IL-6R alpha (sIL-6R alpha) was examined by Western blotting of epithelial cell-depleted colonic tissues. We also investigated whether a soluble gp130-Fc fusion protein could prevent CApC. IL-6 expression was increased in the colon of CC- and CApC-affected mice and was restricted to lamina propria-macrophages. The expression of IL-6R alpha and tumor necrosis factor-alpha converting enzyme was increased in the lamina propria CD11b-macrophages of CC-affected mice. sIL-6R alpha expression was also increased in these tissues. Reduced levels of IL-6R alpha generation were observed in the colonic epithelial cells of CC- and CApC-affected mice and were associated with the increased expression of gp130 and phospho-Stat3. Treatment with soluble gp130Fc significantly reduced the CApC. IL-6 trans-signaling in epithelial cells induced by macrophage-derived IL-6/sIL-6R alpha plays a crucial role in the development of CAC.
Editor: United States: Am Assoc Immnol
Idioma: Inglês

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Essential Roles of IL-6 Trans-Signaling in Colonic Epithelial Cells, Induced by the IL-6/Soluble-IL-6 Receptor Derived from Lamina Propria Macrophages, on the Development of Colitis-Associated Premalignant Cancer in a Murine Model

Matsumoto, Satoshi ; Hara, Taeko ; Mitsuyama, Keiichi ; Yamamoto, Mayuko ; Tsuruta, Osamu ; Sata, Michio ; Scheller, Jurgen ; Rose-John, Stefan ; Kado, Sho-ichi ; Takada, Toshihiko

United States: Am Assoc Immnol

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