期刊
BURNS
卷 43, 期 2, 页码 304-309出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.burns.2016.09.001
关键词
NLRP3 inflammasome; Caspase-1; Interleukin-1 beta; Burns; Mouse model; Pain
资金
- National Health and Medical Research Council (NHMRC) Principle Research Fellowship [AP1059354]
- Australian Research Council Future Fellowships [FT130100361, FT130101215]
- University of Queensland Research Scholarship
The NLRP3 inflammasome is a multi-protein complex that assembles in response to tissue damage or infection, triggering activation of caspase-1, an enzyme that converts interleukin (IL)-1 beta into its active form. A role for the NLRP3 inflammasome is emerging in inflammatory pain, but its influence in other pain types is largely unexamined. Therefore the aim of this study was to assess the role of the NLRP3 inflammasome and its downstream product, caspase-1 in a model of acute burn-induced pain in male mice. A superficial burn was induced on the plantar surface of the left hind paw using a hot plate set at 52.5 C for 25s. Development of burn-induced mechanical allodynia, thermal allodynia, edema and weight bearing changes was assessed in Nlrp3(-/-) and caspase-1-deficient (Ice(-/-))mice, and in mice administered the selective NLRP3 inflammasome inhibitor MCC950. Burn-induced mechanical and thermal allodynia developed normally in NIrp3(-/-) and Ice(-/-) mice and mice administered MCC950. Bum-induced edema was significantly reduced in Ice-/- mice only. Bum-induced weight bearing changes were attenuated in Nirp3(-/-) mice and mice administered MCC950 72h after burn only. This study suggests that NLRP3 and its downstream product caspase-1 have a limited role in the development of burn-induced pain. (C) 2016 Elsevier Ltd and ISBI. All rights reserved.
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