Abstract: Objective: To investigate the effects of deltamethrin (DM) on the intestines and gut microbiota of mice, so as to find out the underlying mechanism of gut-brain axis mediated DM-induced neurotoxicity. Methods: Sixteen 10-week-old male C57BL/6 mice were randomly divided into two groups: the control group and DM exposure group, with 8 mice in each group. The mice in the DM group were administered DM by gavage at 0.1 mL/10 g with a dose of 9.0 mg/kg, while the control group received an equivalent volume of corn oil. Administration was performed once daily for 90 consecutive days. Fecal samples were collected into sterile tubes and frozen immediately one day before the end of exposure. Histopathological changes in hippocampus and colon tissues were observed using hematoxylin-eosin (HE) staining. Nissl staining was applied to observe Nissl bodies in hippocampal neurons. The alterations in gut microbiota were analyzed by using 16S rDNA gene sequencing. Results: Compared to the control group, the body weight of mice in the DM group were increased significantly (P＜0.05). Pathological staining revealed that hippocampal neurons in the DM group showed degeneration, along with reduced and dissolved Nissl bodies. The colonic mucosa exhibited thinning of the muscularis mucosa, shallower crypt depth, reduced goblet cells, and inflammatory cell infiltration. Fecal 16S rDNA sequencing results indicated that, compared with the control group, the abundance of Verrucomicrobiota in the DM group was significantly decreased (P＜0.01) at the phylum level. At the family level, the abundance of Akkermansiaceae in the DM group was decreased (P＜0.01), while the abundance of Ruminococcaceae was increased (P＜0.01). At the genus level, the abundances of genera including Akkermansia in the DM group were decreased (P＜0.05). Conclusion: Subchronic low-dose DM exposure can induce hippocampal neuronal injury, intestinal tissue injury, and gut microbiota dysbiosis in mice. The significant increase in Ruminococcaceae may serve as a potential mechanism underlying DM-induced neurotoxicity.