Abstract
| Original language | English |
|---|---|
| Pages (from-to) | 306-318 |
| Number of pages | 13 |
| Journal | iScience |
| Volume | 6 |
| DOIs | |
| Publication status | Published - 31 Aug 2018 |
Keywords
- Molecular Mechanism of Behavior, Molecular Neuroscience, Medical Microbiology
Cite this
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The ATP Transporter VNUT Mediates Induction of Dectin-1-Triggered Candida Nociception. / Maruyama, Kenta; Takayama, Yasunori; Sugisawa, Erika; Yamanoi, Yu; Yokawa, Takashi; Kondo, Takeshi; Ishibashi, Ken-ichi; Sahoo, Bikash Ranjan; Takemura, Naoki; Mori, Yuki; Kanemaru, Hisashi; Kumagai, Yutaro; Martino, Mikaël M.; Yoshioka, Yoshichika; Nishijo, Hisao; Tanaka, Hiroki; Sasaki, Atsushi; Ohno, Naohito; Iwakura, Yoichiro; Moriyama, Yoshinori; Nomura, Masatoshi; Akira, Shizuo; Tominaga, Makoto.
In: iScience, Vol. 6, 31.08.2018, p. 306-318.Research output: Contribution to journal › Article › Research › peer-review
TY - JOUR
T1 - The ATP Transporter VNUT Mediates Induction of Dectin-1-Triggered Candida Nociception
AU - Maruyama, Kenta
AU - Takayama, Yasunori
AU - Sugisawa, Erika
AU - Yamanoi, Yu
AU - Yokawa, Takashi
AU - Kondo, Takeshi
AU - Ishibashi, Ken-ichi
AU - Sahoo, Bikash Ranjan
AU - Takemura, Naoki
AU - Mori, Yuki
AU - Kanemaru, Hisashi
AU - Kumagai, Yutaro
AU - Martino, Mikaël M.
AU - Yoshioka, Yoshichika
AU - Nishijo, Hisao
AU - Tanaka, Hiroki
AU - Sasaki, Atsushi
AU - Ohno, Naohito
AU - Iwakura, Yoichiro
AU - Moriyama, Yoshinori
AU - Nomura, Masatoshi
AU - Akira, Shizuo
AU - Tominaga, Makoto
PY - 2018/8/31
Y1 - 2018/8/31
N2 - Summary 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 β-glucan stimulated nociceptors depending on Dectin-1, and two pathways in inflammatory pain. The major pathway operates via the Dectin-1-mediated ATP-P2X3/P2X2/3 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. albicans-derived β-glucan has the ability to enhance histamine-independent pruritus, and VNUT inhibitor clodronate can be used to treat unpleasant feelings induced by β-glucan. Collectively, this is the first report to indicate that Dectin-1 and VNUT mediated innate sensory mechanisms that detect fungal infection.
AB - Summary 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 β-glucan stimulated nociceptors depending on Dectin-1, and two pathways in inflammatory pain. The major pathway operates via the Dectin-1-mediated ATP-P2X3/P2X2/3 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. albicans-derived β-glucan has the ability to enhance histamine-independent pruritus, and VNUT inhibitor clodronate can be used to treat unpleasant feelings induced by β-glucan. Collectively, this is the first report to indicate that Dectin-1 and VNUT mediated innate sensory mechanisms that detect fungal infection.
KW - Molecular Mechanism of Behavior, Molecular Neuroscience, Medical Microbiology
U2 - 10.1016/j.isci.2018.08.007
DO - 10.1016/j.isci.2018.08.007
M3 - Article
VL - 6
SP - 306
EP - 318
JO - iScience
JF - iScience
SN - 2589-0042
ER -