Periostin promotes chronic allergic inflammation in response to Th2 cytokines
Allergic inflammation triggered by exposure of an allergen frequently leads to the onset of chronic inflammatory diseases such as atopic dermatitis (AD) and bronchial asthma. The mechanisms underlying chronicity in allergic inflammation remain unresolved. Periostin, a recently characterized matricel...
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| Published in | The Journal of clinical investigation Vol. 122; no. 7; pp. 2590 - 2600 |
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| Main Authors | , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Society for Clinical Investigation
01.07.2012
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0021-9738 1558-8238 1558-8238 |
| DOI | 10.1172/JCI58978 |
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| Abstract | Allergic inflammation triggered by exposure of an allergen frequently leads to the onset of chronic inflammatory diseases such as atopic dermatitis (AD) and bronchial asthma. The mechanisms underlying chronicity in allergic inflammation remain unresolved. Periostin, a recently characterized matricellular protein, interacts with several cell surface integrin molecules, providing signals for tissue development and remodeling. Here we show that periostin is a critical mediator for the amplification and persistence of allergic inflammation using a mouse model of skin inflammation. Th2 cytokines IL-4 and IL-13 stimulated fibroblasts to produce periostin, which interacted with αv integrin, a functional periostin receptor on keratinocytes, inducing production of proinflammatory cytokines, which consequently accelerated Th2-type immune responses. Accordingly, inhibition of periostin or αv integrin prevented the development or progression of allergen-induced skin inflammation. Thus, periostin sets up a vicious circle that links Th2-type immune responses to keratinocyte activation and plays a critical role in the amplification and chronicity of allergic skin inflammation. |
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| AbstractList | Allergic inflammation triggered by exposure of an allergen frequently leads to the onset of chronic inflammatory diseases such as atopic dermatitis (AD) and bronchial asthma. The mechanisms underlying chronicity in allergic inflammation remain unresolved. Periostin, a recently characterized matricellular protein, interacts with several cell surface integrin molecules, providing signals for tissue development and remodeling. Here we show that periostin is a critical mediator for the amplification and persistence of allergic inflammation using a mouse model of skin inflammation. Th2 cytokines IL-4 and IL-13 stimulated fibroblasts to produce periostin, which interacted with [α.sub.v] integrin, a functional periostin receptor on keratinocytes, inducing production of proinflammatory cytokines, which consequently accelerated Th2-type immune responses. Accordingly, inhibition of periostin or [α.sub.v] integrin prevented the development or progression of allergen-induced skin inflammation. Thus, periostin sets up a vicious circle that links Th2-type immune responses to keratinocyte activation and plays a critical role in the amplification and chronicity of allergic skin inflammation. Allergic inflammation triggered by exposure of an allergen frequently leads to the onset of chronic inflammatory diseases such as atopic dermatitis (AD) and bronchial asthma. The mechanisms underlying chronicity in allergic inflammation remain unresolved. Periostin, a recently characterized matricellular protein, interacts with several cell surface integrin molecules, providing signals for tissue development and remodeling. Here we show that periostin is a critical mediator for the amplification and persistence of allergic inflammation using a mouse model of skin inflammation. Th2 cytokines IL-4 and IL-13 stimulated fibroblasts to produce periostin, which interacted with αv integrin, a functional periostin receptor on keratinocytes, inducing production of proinflammatory cytokines, which consequently accelerated Th2-type immune responses. Accordingly, inhibition of periostin or αv integrin prevented the development or progression of allergen-induced skin inflammation. Thus, periostin sets up a vicious circle that links Th2-type immune responses to keratinocyte activation and plays a critical role in the amplification and chronicity of allergic skin inflammation. Allergic inflammation triggered by exposure of an allergen frequently leads to the onset of chronic inflammatory diseases such as atopic dermatitis (AD) and bronchial asthma. The mechanisms underlying chronicity in allergic inflammation remain unresolved. Periostin, a recently characterized matricellular protein, interacts with several cell surface integrin molecules, providing signals for tissue development and remodeling. Here we show that periostin is a critical mediator for the amplification and persistence of allergic inflammation using a mouse model of skin inflammation. Th2 cytokines IL-4 and IL-13 stimulated fibroblasts to produce periostin, which interacted with α^sub v^ integrin, a functional periostin receptor on keratinocytes, inducing production of proinflammatory cytokines, which consequently accelerated Th2-type immune responses. Accordingly, inhibition of periostin or α^sub v^ integrin prevented the development or progression of allergen-induced skin inflammation. Thus, periostin sets up a vicious circle that links Th2-type immune responses to keratinocyte activation and plays a critical role in the amplification and chronicity of allergic skin inflammation. [PUBLICATION ABSTRACT] Allergic inflammation triggered by exposure of an allergen frequently leads to the onset of chronic inflammatory diseases such as atopic dermatitis (AD) and bronchial asthma. The mechanisms underlying chronicity in allergic inflammation remain unresolved. Periostin, a recently characterized matricellular protein, interacts with several cell surface integrin molecules, providing signals for tissue development and remodeling. Here we show that periostin is a critical mediator for the amplification and persistence of allergic inflammation using a mouse model of skin inflammation. Th2 cytokines IL-4 and IL-13 stimulated fibroblasts to produce periostin, which interacted with αv integrin, a functional periostin receptor on keratinocytes, inducing production of proinflammatory cytokines, which consequently accelerated Th2-type immune responses. Accordingly, inhibition of periostin or αv integrin prevented the development or progression of allergen-induced skin inflammation. Thus, periostin sets up a vicious circle that links Th2-type immune responses to keratinocyte activation and plays a critical role in the amplification and chronicity of allergic skin inflammation.Allergic inflammation triggered by exposure of an allergen frequently leads to the onset of chronic inflammatory diseases such as atopic dermatitis (AD) and bronchial asthma. The mechanisms underlying chronicity in allergic inflammation remain unresolved. Periostin, a recently characterized matricellular protein, interacts with several cell surface integrin molecules, providing signals for tissue development and remodeling. Here we show that periostin is a critical mediator for the amplification and persistence of allergic inflammation using a mouse model of skin inflammation. Th2 cytokines IL-4 and IL-13 stimulated fibroblasts to produce periostin, which interacted with αv integrin, a functional periostin receptor on keratinocytes, inducing production of proinflammatory cytokines, which consequently accelerated Th2-type immune responses. Accordingly, inhibition of periostin or αv integrin prevented the development or progression of allergen-induced skin inflammation. Thus, periostin sets up a vicious circle that links Th2-type immune responses to keratinocyte activation and plays a critical role in the amplification and chronicity of allergic skin inflammation. |
| Audience | Academic |
| Author | Kurihara, Yuichi Arima, Kazuhiko Noshiro, Hirokazu Furue, Masutaka Narisawa, Yutaka Toda, Shuji Suzuki, Shoichi Koike, Kenta Ono, Junya Masuoka, Miho Shiraishi, Hiroshi Ohta, Shoichiro Conway, Simon J. Izuhara, Kenji Aoki, Shigehisa Hayashida, Sayaka Inagaki, Naoki Takeuchi, Satoshi |
| AuthorAffiliation | 1 Division of Medical Biochemistry, Department of Biomolecular Sciences, 2 Department of Laboratory Medicine, and 3 Department of Pathology and Biodefense, Saga Medical School, Saga, Japan. 4 Department of Pharmacology, Gifu Pharmaceutical University, Gifu, Japan. 5 Department of Dermatology, Kyushu University, Fukuoka, Japan. 6 Department of Surgery, Saga Medical School, Saga, Japan. 7 Shino-Test Corporation, Sagamihara, Japan. 8 Developmental Biology and Neonatal Medicine Program, HB Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana, USA. 9 Division of Dermatology, Department of Internal Medicine, Saga Medical School, Saga, Japan |
| AuthorAffiliation_xml | – name: 1 Division of Medical Biochemistry, Department of Biomolecular Sciences, 2 Department of Laboratory Medicine, and 3 Department of Pathology and Biodefense, Saga Medical School, Saga, Japan. 4 Department of Pharmacology, Gifu Pharmaceutical University, Gifu, Japan. 5 Department of Dermatology, Kyushu University, Fukuoka, Japan. 6 Department of Surgery, Saga Medical School, Saga, Japan. 7 Shino-Test Corporation, Sagamihara, Japan. 8 Developmental Biology and Neonatal Medicine Program, HB Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana, USA. 9 Division of Dermatology, Department of Internal Medicine, Saga Medical School, Saga, Japan |
| Author_xml | – sequence: 1 givenname: Miho surname: Masuoka fullname: Masuoka, Miho – sequence: 2 givenname: Hiroshi surname: Shiraishi fullname: Shiraishi, Hiroshi – sequence: 3 givenname: Shoichiro surname: Ohta fullname: Ohta, Shoichiro – sequence: 4 givenname: Shoichi surname: Suzuki fullname: Suzuki, Shoichi – sequence: 5 givenname: Kazuhiko surname: Arima fullname: Arima, Kazuhiko – sequence: 6 givenname: Shigehisa surname: Aoki fullname: Aoki, Shigehisa – sequence: 7 givenname: Shuji surname: Toda fullname: Toda, Shuji – sequence: 8 givenname: Naoki surname: Inagaki fullname: Inagaki, Naoki – sequence: 9 givenname: Yuichi surname: Kurihara fullname: Kurihara, Yuichi – sequence: 10 givenname: Sayaka surname: Hayashida fullname: Hayashida, Sayaka – sequence: 11 givenname: Satoshi surname: Takeuchi fullname: Takeuchi, Satoshi – sequence: 12 givenname: Kenta surname: Koike fullname: Koike, Kenta – sequence: 13 givenname: Junya surname: Ono fullname: Ono, Junya – sequence: 14 givenname: Hirokazu surname: Noshiro fullname: Noshiro, Hirokazu – sequence: 15 givenname: Masutaka surname: Furue fullname: Furue, Masutaka – sequence: 16 givenname: Simon J. surname: Conway fullname: Conway, Simon J. – sequence: 17 givenname: Yutaka surname: Narisawa fullname: Narisawa, Yutaka – sequence: 18 givenname: Kenji surname: Izuhara fullname: Izuhara, Kenji |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22684102$$D View this record in MEDLINE/PubMed |
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| Title | Periostin promotes chronic allergic inflammation in response to Th2 cytokines |
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