期刊
ACTA DERMATO-VENEREOLOGICA
卷 97, 期 8, 页码 922-927出版社
ACTA DERMATO-VENEREOLOGICA
DOI: 10.2340/00015555-2697
关键词
itch; leukotriene B-4; interleukin-31; keratinocytes; scratching; dorsal root ganglia
类别
资金
- Japan Agency for Medical Research and Development (AMED)
- Chugai Pharmaceutical Co. Ltd.
- Platform Project
A recent study suggests that interleukin-31 (IL-31) exerts its effect via indirect mechanisms rather than through direct stimulation of cutaneous nerves. However, the underlying peripheral mechanisms of IL-31-induced itch in the skin remain unclear. Therefore, the present study investigated the peripheral mechanisms underlying IL-31-induced itch in mice. IL-31-induced itch-related response was inhibited by anti-allergic drugs (tranilast and azelastine), but not by an H-1 histamine receptor antagonist (terfenadine). Furthermore, a 5-lipoxygenase inhibitor (zileuton), but not a cyclooxygenase inhibitor (indomethacin), and a leuko-triene B-4 (LTB4) receptor antagonist (CMHVA) attenuated the action of IL-31. IL-31 receptor-immunoreactivity was observed in the epidermis and primary sensory neurones. IL-31 receptor mRNA was expressed in mouse keratinocytes and dorsal root ganglia neurones. IL-31 increased the production of LTB4 in mouse keratinocytes. These results suggest that IL-31 elicits itch not only through direct action on primary sensory neurones, but also by inducing LTB4 production in keratinocytes.
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