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Integrated Analysis of Midgut Transcriptome and Microbiome Reveals That Manganese‐Induced Dysbiosis Drives Metabolic Disruption and Developmental Toxicity in Bombyx mori

Lei Xin; Yazhen Chen; Delong Guan; Lida Huang; Yiwei Lv; Wantao Rong; Xiaodong Li
Environmental Microbiology · Vol. 28, Issue 1 · 2026

Abstract

Manganese (Mn) contamination poses a significant environmental threat, yet the mechanisms underlying its toxicity remain poorly characterised. Here, we used an integrative multi‐omics approach to elucidate how dietary Mn disrupts the gut‐microbiome axis in the silkworm, Bombyx mori . High‐dose Mn exposure triggered severe, dose‐dependent growth retardation, reducing larval weight by 55.1%. This was concurrent with profound gut microbiome dysbiosis, evidenced by reduced bacterial diversity, community homogenisation and a sharp decline in beneficial genera such as Delftia , alongside the complete elimination of key commensals like Bifidobacterium . Host midgut transcriptomics revealed 1255 differentially expressed genes, with significant upregulation of detoxification and stress pathways and marked suppression of genes involved in nutrient metabolism. Critically, integrative analysis demonstrated a strong correlation between microbiome disruption and host metabolic gene expression, suggesting that Mn toxicity operates by disrupting the gut microbiome‐host metabolic axis. Our findings provide crucial mechanistic insights into heavy metal ecotoxicology and highlight the vulnerability of beneficial insect‐microbe symbioses to environmental contamination, with important implications for sustainable agriculture in metal‐polluted regions.

Bibliographic Information

JournalEnvironmental Microbiology
PublisherWiley
Publication Date2026-01-01
Publication Year2026
Volume28
Issue1
Document TypeJournal Article
Print ISSN1462-2912
eISSN1462-2920
DOI10.1111/1462-2920.70223
SubjectMicrobial Ecology

Access Information

NARA Access Coverage1999-01-01~Current
Journal Homepagehttps://onlinelibrary.wiley.com/loi/14622920
Publisher PageOpen Publisher Page
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