Effects of exposure to the neonicotinoid pesticide clothianidin on α-defensin secretion and gut microbiota in mice

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–p...

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Published in:Journal of Veterinary Medical Science 2024, Vol.86(3), pp.277-284
Main Authors: 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
Format: Article
Language:English
Subjects:
Cecum
clothianidin
Defensins
Dysbacteriosis
dysbiosis
Ileum
Intestinal microflora
Intestine
Jejunum
Microbiota
neonicotinoid
Paneth cells
Pesticides
Toxicology
α-defensin
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Summary: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.
ISSN:0916-7250
1347-7439
DOI:10.1292/jvms.23-0514