Pulmonary suppressor of cytokine signaling-1 induced by IL-13 regulates allergic asthma phenotype

Satoru Fukuyama, Takako Nakano, Takafumi Matsumoto, Brian G.G. Oliver, Janette K. Burgess, Atsushi Moriwaki, Kentaro Tanaka, Masato Kubo, Tomoaki Hoshino, Hiroyuki Tanaka, Andrew N.J. McKenzie, Koichiro Matsumoto, Hisamichi Aizawa, Yoichi Nakanishi, Akihiko Yoshimura, Judith L. Black, Hiromasa Inoue

研究成果: ジャーナルへの寄稿記事

25 引用 (Scopus)

抄録

Rationale: Th2 cytokines play an important role in allergic diseases. These cytokines activate signal transduction pathways, including Janus kinase/signal transducer and activator of transcription (STAT) signaling. Although the suppressor of cytokine signaling (SOCS) family protein, a negative regulator of the Janus kinase/STAT signaling pathway, contributes to helper T cell differentiation during immune responses, the role of SOCS proteins within the structural cells of a target organ has not been clarified in allergy. Objectives: To study the local function of SOCS in the development of asthma. Methods: We used mouse models of IL-13- and ovalbumin (OVA)-induced allergic airway disease. Airway smooth muscle cells were cultured from patients with asthma. Measurements and Main Results: The administration of IL-13 induced not only airway responses but also SOCS1 expression at the local inflammatory site. The up-regulated SOCS1 markedly suppressed IL-13-dependent STAT6 activation and eotaxin expression and subsequently down-regulated IL-13-induced airway inflammatory responses. The inactivation of SOCS1 induced airway hyperresponsiveness after IL-13 treatment even in hyporesponsive C57BL/6 background mice. In an OVA-induced model of allergic airway disease, allergen exposure up-regulated local SOCS1 expression, and the induction of SOCS1 in the airways attenuated allergen-induced airway responses. Inactivation of IL-13 inhibited SOCS1 induction in a model of allergic airway disease. Interestingly, airway smooth muscle cells from individuals with asthma had impaired upregulation of SOCS1 after IL-13 stimulation. Conclusions: SOCS1 induction by IL-13 in airway structural cells is critical to negatively control allergic airway disease.

元の言語英語
ページ(範囲)992-998
ページ数7
ジャーナルAmerican Journal of Respiratory and Critical Care Medicine
179
発行部数11
DOI
出版物ステータス出版済み - 6 1 2009

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Interleukin-13
Asthma
Cytokines
Phenotype
Lung
Suppressor of Cytokine Signaling Proteins
Janus Kinases
Ovalbumin
Transducers
Allergens
Smooth Muscle Myocytes
Airway Management
Helper-Inducer T-Lymphocytes
Cell Differentiation
Signal Transduction
Hypersensitivity
Up-Regulation

All Science Journal Classification (ASJC) codes

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine

これを引用

Pulmonary suppressor of cytokine signaling-1 induced by IL-13 regulates allergic asthma phenotype. / Fukuyama, Satoru; Nakano, Takako; Matsumoto, Takafumi; Oliver, Brian G.G.; Burgess, Janette K.; Moriwaki, Atsushi; Tanaka, Kentaro; Kubo, Masato; Hoshino, Tomoaki; Tanaka, Hiroyuki; McKenzie, Andrew N.J.; Matsumoto, Koichiro; Aizawa, Hisamichi; Nakanishi, Yoichi; Yoshimura, Akihiko; Black, Judith L.; Inoue, Hiromasa.

:: American Journal of Respiratory and Critical Care Medicine, 巻 179, 番号 11, 01.06.2009, p. 992-998.

研究成果: ジャーナルへの寄稿記事

Fukuyama, S, Nakano, T, Matsumoto, T, Oliver, BGG, Burgess, JK, Moriwaki, A, Tanaka, K, Kubo, M, Hoshino, T, Tanaka, H, McKenzie, ANJ, Matsumoto, K, Aizawa, H, Nakanishi, Y, Yoshimura, A, Black, JL & Inoue, H 2009, 'Pulmonary suppressor of cytokine signaling-1 induced by IL-13 regulates allergic asthma phenotype', American Journal of Respiratory and Critical Care Medicine, 巻. 179, 番号 11, pp. 992-998. https://doi.org/10.1164/rccm.200806-992OC
Fukuyama, Satoru ; Nakano, Takako ; Matsumoto, Takafumi ; Oliver, Brian G.G. ; Burgess, Janette K. ; Moriwaki, Atsushi ; Tanaka, Kentaro ; Kubo, Masato ; Hoshino, Tomoaki ; Tanaka, Hiroyuki ; McKenzie, Andrew N.J. ; Matsumoto, Koichiro ; Aizawa, Hisamichi ; Nakanishi, Yoichi ; Yoshimura, Akihiko ; Black, Judith L. ; Inoue, Hiromasa. / Pulmonary suppressor of cytokine signaling-1 induced by IL-13 regulates allergic asthma phenotype. :: American Journal of Respiratory and Critical Care Medicine. 2009 ; 巻 179, 番号 11. pp. 992-998.
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title = "Pulmonary suppressor of cytokine signaling-1 induced by IL-13 regulates allergic asthma phenotype",
abstract = "Rationale: Th2 cytokines play an important role in allergic diseases. These cytokines activate signal transduction pathways, including Janus kinase/signal transducer and activator of transcription (STAT) signaling. Although the suppressor of cytokine signaling (SOCS) family protein, a negative regulator of the Janus kinase/STAT signaling pathway, contributes to helper T cell differentiation during immune responses, the role of SOCS proteins within the structural cells of a target organ has not been clarified in allergy. Objectives: To study the local function of SOCS in the development of asthma. Methods: We used mouse models of IL-13- and ovalbumin (OVA)-induced allergic airway disease. Airway smooth muscle cells were cultured from patients with asthma. Measurements and Main Results: The administration of IL-13 induced not only airway responses but also SOCS1 expression at the local inflammatory site. The up-regulated SOCS1 markedly suppressed IL-13-dependent STAT6 activation and eotaxin expression and subsequently down-regulated IL-13-induced airway inflammatory responses. The inactivation of SOCS1 induced airway hyperresponsiveness after IL-13 treatment even in hyporesponsive C57BL/6 background mice. In an OVA-induced model of allergic airway disease, allergen exposure up-regulated local SOCS1 expression, and the induction of SOCS1 in the airways attenuated allergen-induced airway responses. Inactivation of IL-13 inhibited SOCS1 induction in a model of allergic airway disease. Interestingly, airway smooth muscle cells from individuals with asthma had impaired upregulation of SOCS1 after IL-13 stimulation. Conclusions: SOCS1 induction by IL-13 in airway structural cells is critical to negatively control allergic airway disease.",
author = "Satoru Fukuyama and Takako Nakano and Takafumi Matsumoto and Oliver, {Brian G.G.} and Burgess, {Janette K.} and Atsushi Moriwaki and Kentaro Tanaka and Masato Kubo and Tomoaki Hoshino and Hiroyuki Tanaka and McKenzie, {Andrew N.J.} and Koichiro Matsumoto and Hisamichi Aizawa and Yoichi Nakanishi and Akihiko Yoshimura and Black, {Judith L.} and Hiromasa Inoue",
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AU - Fukuyama, Satoru

AU - Nakano, Takako

AU - Matsumoto, Takafumi

AU - Oliver, Brian G.G.

AU - Burgess, Janette K.

AU - Moriwaki, Atsushi

AU - Tanaka, Kentaro

AU - Kubo, Masato

AU - Hoshino, Tomoaki

AU - Tanaka, Hiroyuki

AU - McKenzie, Andrew N.J.

AU - Matsumoto, Koichiro

AU - Aizawa, Hisamichi

AU - Nakanishi, Yoichi

AU - Yoshimura, Akihiko

AU - Black, Judith L.

AU - Inoue, Hiromasa

PY - 2009/6/1

Y1 - 2009/6/1

N2 - Rationale: Th2 cytokines play an important role in allergic diseases. These cytokines activate signal transduction pathways, including Janus kinase/signal transducer and activator of transcription (STAT) signaling. Although the suppressor of cytokine signaling (SOCS) family protein, a negative regulator of the Janus kinase/STAT signaling pathway, contributes to helper T cell differentiation during immune responses, the role of SOCS proteins within the structural cells of a target organ has not been clarified in allergy. Objectives: To study the local function of SOCS in the development of asthma. Methods: We used mouse models of IL-13- and ovalbumin (OVA)-induced allergic airway disease. Airway smooth muscle cells were cultured from patients with asthma. Measurements and Main Results: The administration of IL-13 induced not only airway responses but also SOCS1 expression at the local inflammatory site. The up-regulated SOCS1 markedly suppressed IL-13-dependent STAT6 activation and eotaxin expression and subsequently down-regulated IL-13-induced airway inflammatory responses. The inactivation of SOCS1 induced airway hyperresponsiveness after IL-13 treatment even in hyporesponsive C57BL/6 background mice. In an OVA-induced model of allergic airway disease, allergen exposure up-regulated local SOCS1 expression, and the induction of SOCS1 in the airways attenuated allergen-induced airway responses. Inactivation of IL-13 inhibited SOCS1 induction in a model of allergic airway disease. Interestingly, airway smooth muscle cells from individuals with asthma had impaired upregulation of SOCS1 after IL-13 stimulation. Conclusions: SOCS1 induction by IL-13 in airway structural cells is critical to negatively control allergic airway disease.

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