期刊
ISCIENCE
卷 6, 期 -, 页码 306-+出版社
CELL PRESS
DOI: 10.1016/j.isci.2018.08.007
关键词
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资金
- Osaka University MEET project
- Takeda Science Foundation
- KAKENHI [JP26670663, JP16K15665, JP15H05686, 18H02970]
- Translational Research Network Program from Japan Agency for Medical Research and Development AMED
- Japan Intractable Diseases Research Foundation
- Senri Life Science Foundation
- Japan Prize Foundation
- Mochida Memorial Foundation
- National Institute for Physiological Science
- Japan Rheumatism Foundation
- Akashi Medical Research Foundation
- Kanzawa Medical Research Foundation
- Terumo Foundation for Life Sciences and Arts
- Life Science Foundation
- Osaka University International Joint Research Promotion Program
- Grants-in-Aid for Scientific Research [18H02970] Funding Source: KAKEN
Candida albicans infection can cause skin, vulvar, or oral pain. Despite the obvious algesic activity of C. albicans, the molecular mechanisms of fungal nociception remain largely unknown. Here we show that the C albicans-specific signaling pathway led to severe mechanical allodynia. We discovered that C. albicans-derived beta-glucan stimulated nociceptors depending on Dectin-1, and two pathways in inflammatory pain. The major pathway operates via the Dectin-1-mediated ATP-P2X(3)/P2X(2/3) axis through intercellular relationships between keratinocytes and primary sensory neurons, which depends on the ATP transporter vesicular nucleotide transporter (VNUT). The other pathway operates via the Dectin-1-mediated PLC-TRPV1/TRPA1 axis in primary sensory neurons. Intriguingly, C. albicansderived beta-glucan has the ability to enhance histamine-independent pruritus, and VNUT inhibitor clodronate can be used to treat unpleasant feelings induced by beta-glucan. Collectively, this is the first report to indicate that Dectin-1 and VNUT mediated innate sensory mechanisms that detect fungal infection.
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