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Interleukin-33 mediates formalin-induced inflammatory pain in mice
- Source :
- Neuroscience. 241
- Publication Year :
- 2013
-
Abstract
- 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.
- Subjects :
- MAPK/ERK pathway
Allergy
medicine.medical_treatment
Interleukin-1 Receptor-Like 1 Protein
Arthritis
Pain
Mice
Formaldehyde
Medicine
Animals
Receptor
Inflammation
Mice, Knockout
Mice, Inbred BALB C
Behavior, Animal
business.industry
General Neuroscience
Interleukins
Receptors, Interleukin
medicine.disease
Interleukin-33
Interleukin 33
Cytokine
Immunology
Irritants
business
Licking
Signal Transduction
Subjects
Details
- ISSN :
- 18737544
- Volume :
- 241
- Database :
- OpenAIRE
- Journal :
- Neuroscience
- Accession number :
- edsair.doi.dedup.....0ceca2177e355ece80b09cf201441654