Clock-dependent temporal regulation of IL-33/ST2-mediated mast cell response

Takahiro Kawauchi, Kayoko Ishimaru, Yuki Nakamura, Nobuhiro Nakano, Mutsuko Hara, Hideoki Ogawa, Ko Okumura, Shigenobu Shibata, Atsuhito Nakao

    研究成果: Article

    7 引用 (Scopus)

    抄録

    Background: Interleukin-33 (IL-33) is an alarmin cytokine that binds to the interleukin 1 receptor-like 1 protein ST2. Clock is a key circadian gene that is essential for endogenous clockworks in mammals. This study investigated whether Clock temporally regulated IL-33-mediated responses in mast cells. Methods: The kinetics of IL-33-mediated IL-6, IL-13, and TNF-α productions were compared between bone marrow-derived mast cells (BMMCs) from wild-type and Clock-mutated mice (Clock δ19/δ19 mice). The kinetics of the neutrophil influx into the peritoneal cavity or expression of IL-13 and Gob-5 in the lung in response to IL-33 were compared between wild-type and Clock δ19/δ19 mice. We also examined the kinetics of ST2 expression in mast cells and its association with Clock expression. Results: There was a time-of-day-dependent variation in IL-33-mediated IL-6, IL-13, and TNF-α production in wild-type BMMCs, which was absent in Clock-mutated BMMCs. IL-33-induced neutrophil infiltration into the peritoneal cavity also showed a time-of-day-dependent variation in wild-type mice, which was absent in Clock δ19/δ19 mice. Furthermore, IL-33-induced IL-13 and Gob-5 expression in the lung exhibited a time-of-day-dependent variation in wild-type mice. These temporal variations in IL-33-mediated mast cell responses were associated with temporal variations of ST2 expression in mast cells. In addition, CLOCK bound to the promoter region of ST2 and Clock deletion resulted in down-regulation of ST2 expression in mast cells. Conclusions: CLOCK temporally gates mast cell responses to IL-33 via regulation of ST2 expression. Our findings provide novel insights into IL-33/mast cell-associated physiology and pathologies.

    元の言語English
    ジャーナルAllergology International
    DOI
    出版物ステータスAccepted/In press - 2016 9 5

    Fingerprint

    Mast Cells
    Interleukin-13
    Bone Marrow
    Peritoneal Cavity
    Interleukin-6
    Interleukin-33
    Cell Physiological Phenomena
    Lung
    Neutrophil Infiltration
    Essential Genes
    Genetic Promoter Regions
    Mammals
    Neutrophils
    Down-Regulation
    Pathology
    Cytokines

    ASJC Scopus subject areas

    • Immunology and Allergy

    これを引用

    Kawauchi, T., Ishimaru, K., Nakamura, Y., Nakano, N., Hara, M., Ogawa, H., ... Nakao, A. (受理済み/印刷中). Clock-dependent temporal regulation of IL-33/ST2-mediated mast cell response. Allergology International. https://doi.org/10.1016/j.alit.2017.02.004

    Clock-dependent temporal regulation of IL-33/ST2-mediated mast cell response. / Kawauchi, Takahiro; Ishimaru, Kayoko; Nakamura, Yuki; Nakano, Nobuhiro; Hara, Mutsuko; Ogawa, Hideoki; Okumura, Ko; Shibata, Shigenobu; Nakao, Atsuhito.

    :: Allergology International, 05.09.2016.

    研究成果: Article

    Kawauchi, Takahiro ; Ishimaru, Kayoko ; Nakamura, Yuki ; Nakano, Nobuhiro ; Hara, Mutsuko ; Ogawa, Hideoki ; Okumura, Ko ; Shibata, Shigenobu ; Nakao, Atsuhito. / Clock-dependent temporal regulation of IL-33/ST2-mediated mast cell response. :: Allergology International. 2016.
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    title = "Clock-dependent temporal regulation of IL-33/ST2-mediated mast cell response",
    abstract = "Background: Interleukin-33 (IL-33) is an alarmin cytokine that binds to the interleukin 1 receptor-like 1 protein ST2. Clock is a key circadian gene that is essential for endogenous clockworks in mammals. This study investigated whether Clock temporally regulated IL-33-mediated responses in mast cells. Methods: The kinetics of IL-33-mediated IL-6, IL-13, and TNF-α productions were compared between bone marrow-derived mast cells (BMMCs) from wild-type and Clock-mutated mice (Clock δ19/δ19 mice). The kinetics of the neutrophil influx into the peritoneal cavity or expression of IL-13 and Gob-5 in the lung in response to IL-33 were compared between wild-type and Clock δ19/δ19 mice. We also examined the kinetics of ST2 expression in mast cells and its association with Clock expression. Results: There was a time-of-day-dependent variation in IL-33-mediated IL-6, IL-13, and TNF-α production in wild-type BMMCs, which was absent in Clock-mutated BMMCs. IL-33-induced neutrophil infiltration into the peritoneal cavity also showed a time-of-day-dependent variation in wild-type mice, which was absent in Clock δ19/δ19 mice. Furthermore, IL-33-induced IL-13 and Gob-5 expression in the lung exhibited a time-of-day-dependent variation in wild-type mice. These temporal variations in IL-33-mediated mast cell responses were associated with temporal variations of ST2 expression in mast cells. In addition, CLOCK bound to the promoter region of ST2 and Clock deletion resulted in down-regulation of ST2 expression in mast cells. Conclusions: CLOCK temporally gates mast cell responses to IL-33 via regulation of ST2 expression. Our findings provide novel insights into IL-33/mast cell-associated physiology and pathologies.",
    keywords = "CLOCK, Cytokine, IL-33, Mast cells, ST2",
    author = "Takahiro Kawauchi and Kayoko Ishimaru and Yuki Nakamura and Nobuhiro Nakano and Mutsuko Hara and Hideoki Ogawa and Ko Okumura and Shigenobu Shibata and Atsuhito Nakao",
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    TY - JOUR

    T1 - Clock-dependent temporal regulation of IL-33/ST2-mediated mast cell response

    AU - Kawauchi, Takahiro

    AU - Ishimaru, Kayoko

    AU - Nakamura, Yuki

    AU - Nakano, Nobuhiro

    AU - Hara, Mutsuko

    AU - Ogawa, Hideoki

    AU - Okumura, Ko

    AU - Shibata, Shigenobu

    AU - Nakao, Atsuhito

    PY - 2016/9/5

    Y1 - 2016/9/5

    N2 - Background: Interleukin-33 (IL-33) is an alarmin cytokine that binds to the interleukin 1 receptor-like 1 protein ST2. Clock is a key circadian gene that is essential for endogenous clockworks in mammals. This study investigated whether Clock temporally regulated IL-33-mediated responses in mast cells. Methods: The kinetics of IL-33-mediated IL-6, IL-13, and TNF-α productions were compared between bone marrow-derived mast cells (BMMCs) from wild-type and Clock-mutated mice (Clock δ19/δ19 mice). The kinetics of the neutrophil influx into the peritoneal cavity or expression of IL-13 and Gob-5 in the lung in response to IL-33 were compared between wild-type and Clock δ19/δ19 mice. We also examined the kinetics of ST2 expression in mast cells and its association with Clock expression. Results: There was a time-of-day-dependent variation in IL-33-mediated IL-6, IL-13, and TNF-α production in wild-type BMMCs, which was absent in Clock-mutated BMMCs. IL-33-induced neutrophil infiltration into the peritoneal cavity also showed a time-of-day-dependent variation in wild-type mice, which was absent in Clock δ19/δ19 mice. Furthermore, IL-33-induced IL-13 and Gob-5 expression in the lung exhibited a time-of-day-dependent variation in wild-type mice. These temporal variations in IL-33-mediated mast cell responses were associated with temporal variations of ST2 expression in mast cells. In addition, CLOCK bound to the promoter region of ST2 and Clock deletion resulted in down-regulation of ST2 expression in mast cells. Conclusions: CLOCK temporally gates mast cell responses to IL-33 via regulation of ST2 expression. Our findings provide novel insights into IL-33/mast cell-associated physiology and pathologies.

    AB - Background: Interleukin-33 (IL-33) is an alarmin cytokine that binds to the interleukin 1 receptor-like 1 protein ST2. Clock is a key circadian gene that is essential for endogenous clockworks in mammals. This study investigated whether Clock temporally regulated IL-33-mediated responses in mast cells. Methods: The kinetics of IL-33-mediated IL-6, IL-13, and TNF-α productions were compared between bone marrow-derived mast cells (BMMCs) from wild-type and Clock-mutated mice (Clock δ19/δ19 mice). The kinetics of the neutrophil influx into the peritoneal cavity or expression of IL-13 and Gob-5 in the lung in response to IL-33 were compared between wild-type and Clock δ19/δ19 mice. We also examined the kinetics of ST2 expression in mast cells and its association with Clock expression. Results: There was a time-of-day-dependent variation in IL-33-mediated IL-6, IL-13, and TNF-α production in wild-type BMMCs, which was absent in Clock-mutated BMMCs. IL-33-induced neutrophil infiltration into the peritoneal cavity also showed a time-of-day-dependent variation in wild-type mice, which was absent in Clock δ19/δ19 mice. Furthermore, IL-33-induced IL-13 and Gob-5 expression in the lung exhibited a time-of-day-dependent variation in wild-type mice. These temporal variations in IL-33-mediated mast cell responses were associated with temporal variations of ST2 expression in mast cells. In addition, CLOCK bound to the promoter region of ST2 and Clock deletion resulted in down-regulation of ST2 expression in mast cells. Conclusions: CLOCK temporally gates mast cell responses to IL-33 via regulation of ST2 expression. Our findings provide novel insights into IL-33/mast cell-associated physiology and pathologies.

    KW - CLOCK

    KW - Cytokine

    KW - IL-33

    KW - Mast cells

    KW - ST2

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    DO - 10.1016/j.alit.2017.02.004

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