| Item type |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2026-02-25 |
| タイトル |
|
|
タイトル |
Sub-acute oral exposure to lowest observed adverse effect level of nivalenol exacerbates atopic dermatitis in mice via direct activation of mitogen-activated protein kinase signal in antigen-presenting cells |
|
言語 |
en |
| 言語 |
|
|
言語 |
eng |
| 資源タイプ |
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|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
|
資源タイプ |
journal article |
| 著者 |
Matsuzaka, Reo
Yamaguchi, Hiroki
Ohira, Chiharu
Kurita, Tomoe
Iwashita, Naoki
Takagi, Yoshiichi
Nishino, Tomomi
Noda, Kyoko
Sugita, Kazutoshi
Kushiro, Masayo
Miyake, Shiro
Fukuyama, Tomoki
|
| Abstract |
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内容記述タイプ |
Abstract |
|
内容記述 |
This study investigated the immunotoxic effects of the mycotoxin nivalenol (NIV) using antigen-presenting cells and a mouse model of atopic dermatitis (AD). In vitro experiments were conducted using a mouse macrophage cell line (RAW 264.7) and mouse dendritic cell line (DC 2.4). After cells were exposed to NIV (0.19-5 µmol) for 24 h, the production of pro-inflammatory cytokines (IL-1β, IL-6, and TNFα) was quantified. To further investigate the inflammatory cytokine production pathway, the possible involvement of mitogen-activated protein kinase (MAPK) pathways, such as ERK1/2, p-38, and JNK, in NIV exposure was analyzed using MAPK inhibitors and phosphorylation analyses. In addition, the pro-inflammatory effects of oral exposure to NIV at low concentrations (1 or 5 ppm) were evaluated in an NC/Nga mouse model of hapten-induced AD. In vitro experiments demonstrated that exposure to NIV significantly enhanced the production of TNFα. In addition, it also directly induced the phosphorylation of MAPK, indicated by the inhibition of TNFα production following pretreatment with MAPK inhibitors. Oral exposure to NIV significantly exacerbated the symptoms of AD, including a significant increase in helper T cells and IgE-produced B cells in auricular lymph nodes and secretion of pro-inflammatory cytokines, such as IL-4, IL-5, and IL-13, compared with the vehicle control group. Our findings indicate that exposure to NIV directly enhanced the phosphorylation of ERK1/2, p-38, and JNK, resulting in a significant increase in TNFα production in antigen-presenting cells, which is closely related to the development of atopic dermatitis. |
|
言語 |
en |
| 書誌情報 |
Archives of Toxicology
巻 98,
号 7,
p. 2173-2183,
発行日 2024-04-14
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| 出版者 |
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出版者 |
Springer Nature |
| DOI |
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|
識別子タイプ |
DOI |
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関連識別子 |
10.1007/s00204-024-03740-3 |
| 著者版フラグ |
|
|
出版タイプ |
AM |
|
出版タイプResource |
http://purl.org/coar/version/c_ab4af688f83e57aa |
| 査読 |
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|
内容記述タイプ |
Other |
|
内容記述 |
査読あり |
ATOX-S-24-00326.pdf (1 MB)
