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

• Published in: Journal of Veterinary Medical Science Vol. 86; no. 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: Journal Article
• Language: English
• Published: Japan JAPANESE SOCIETY OF VETERINARY SCIENCE 01.03.2024; Japan Science and Technology Agency; The Japanese Society of Veterinary Science
• Subjects: Cecum; clothianidin; Defensins; Dysbacteriosis; dysbiosis; Ileum; Intestinal microflora; Intestine; Jejunum; Microbiota; neonicotinoid; Paneth cells; Pesticides; Toxicology; α-defensin; microbiota; α-defensin; neonicotinoid; clothianidin; dysbiosis
• ISSN: 0916-7250; 1347-7439; 1347-7439
• DOI: 10.1292/jvms.23-0514

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.