期刊
NEUROSCIENCE
卷 241, 期 -, 页码 59-66出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2013.03.019
关键词
interleukin-33; ST2; pain; formalin test
资金
- National Natural Science Foundation of China [31000495, 30970975]
- Research Fund for the Doctoral Program of Higher Education of China [20100071120046, 20100071120042]
- National Key Basic Research Program of China [2013CB531906]
- Fundamental Research Funds for the Central Universities, China
- Young Scientist Foundation of Fudan University, China
Interleukin-33 (IL-33), a member of the IL-1 family, has attracted growing interest since its discovery in 2003. IL-33 has been implicated in many diseases, including arthritis, asthma, allergies, and cardiovascular and infectious diseases. However, few studies have investigated its role in the transmission and modulation of pain. The present study was designed to explore the possible roles of IL-33 and its receptor, ST2, in formalin-induced inflammatory pain in mice. We found that both subcutaneous (s.c., 300 ng) and intrathecal injection (i.t., 3 ng) of recombinant IL-33 (rIL-33) increased paw lifting and licking time not only in normal mice but also in formalin models. Administration of ST2 antibody, which blocked the IL-33/ST2 signaling, alleviated the formalin-induced spontaneous pain behavior. Moreover, the ST2(-/-) mice showed significantly decreased pain behavior, as well as reduced ultrasonic vocalization induced by formalin, compared with the wild-type group. Additionally, ST2 antibody alleviated the potentiating effects of rIL-33 on pain behavior in the formalin mice, indicating that IL-33 plays a role in pain modulation through its ST2 receptor. These data suggest IL-33 and its ST2 receptor mediate formalin-induced inflammatory pain, and as a result this cytokine and its receptor may be new targets for the development of analgesics. (c) 2013 IBRO. Published by Elsevier Ltd. All rights reserved.
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