Yonoichi Sakura, Hara Yukako, Ishida Yuya, Shoda Asuka, Kimura Mako, Murata Midori, Nunobiki Sarika, Ito Makiko, Yoshimoto Ayano, Mantani Youhei, Yokoyama Toshifumi, Hirano Tetsushi, Ikenaka Yoshinori, Yokoi Yuki, Ayabe Tokiyoshi, Nakamura Kiminori, Hoshi Nobuhiko
Laboratory of Animal Molecular Morphology, Department of Animal Science, Graduate School of Agricultural Science, Kobe University, Hyogo, Japan.
Laboratory of Histophysiology, Department of Animal Science, Graduate School of Agricultural Science, Kobe University, Hyogo, Japan.
J Vet Med Sci. 2024 Mar 1;86(3):277-284. doi: 10.1292/jvms.23-0514. Epub 2024 Jan 23.
The mechanism by which the neonicotinoid pesticide clothianidin (CLO) disrupts the intestinal microbiota of experimental animals is unknown. We focused on α-defensins, which are regulators of the intestinal microbiota. Subchronic exposure to CLO induced dysbiosis and reduced short-chain fatty acid-producing bacteria in the intestinal microbiota of mice. Levels of cryptdin-1 (Crp1, a major α-defensin in mice) in feces and cecal contents were lower in the CLO-exposed groups than in control. In Crp1 immunostaining, Paneth cells in the jejunum and ileum of the no-observed-adverse-effect-level CLO-exposed group showed a stronger positive signal than control, likely due to the suppression of Crp1 release. Our results showed that CLO exposure suppresses α-defensin secretion from Paneth cells as part of the mechanism underlying CLO-induced dysbiosis.
新烟碱类杀虫剂噻虫胺（CLO）破坏实验动物肠道微生物群的机制尚不清楚。我们聚焦于α-防御素，其为肠道微生物群的调节剂。亚慢性暴露于CLO会导致小鼠肠道微生物群失调，并减少产生短链脂肪酸的细菌。暴露于CLO的组中，粪便和盲肠内容物中隐窝防御素-1（Crp1，小鼠中的一种主要α-防御素）的水平低于对照组。在Crp1免疫染色中，未观察到不良影响水平的CLO暴露组空肠和回肠中的潘氏细胞显示出比对照组更强的阳性信号，这可能是由于Crp1释放受到抑制。我们的结果表明，作为CLO诱导的失调潜在机制的一部分，暴露于CLO会抑制潘氏细胞分泌α-防御素。
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