2025-05-01 カリフォルニア大学ロサンゼルス校(UCLA)
<関連情報>
- https://newsroom.ucla.edu/releases/reducing-mercury-absorption-food
- https://www.cell.com/cell-host-microbe/abstract/S1931-3128(25)00142-8
人工腸内細菌が妊娠マウスの食事性メチル水銀曝露から保護する An engineered gut bacterium protects against dietary methylmercury exposure in pregnant mice
Kristie B. Yu ∙ Franciscus Chandra ∙ Elena J. Coley-O’Rourke ∙ … ∙ Tien S. Dong ∙ Amina T. Schartup ∙ Elaine Y. Hsiao
Cell Host & Microb Published:May 1, 2025
DOI:https://doi.org/10.1016/j.chom.2025.04.009
Graphical abstract
Highlights
- Engineered gut commensal B. thetaiotaomicron confers MeHg demethylation activity
- BtmerA/B decreases MeHg in gut lumen of adult monocolonized mice exposed to MeHg
- BtmerA/B lowers MeHg in dams and fetuses, reducing harmful effects during pregnancy
Summary
Despite efforts to decrease mercury emissions, chronic exposure to the neurotoxicant methylmercury (MeHg) continues to be a global problem that contributes to disparities in risk for neurological and metabolic diseases. Herein we engineer a human commensal gut bacterium, Bacteroides thetaiotaomicron (Bt), to detoxify MeHg by heterologous expression of organomercury lyase (MerB) and mercuric reductase (MerA) genes derived from a resistant bacterium isolated from Hg-polluted mines. We demonstrate that BtmerA/B demethylates MeHg both in vitro and within the intestines of mice orally exposed to MeHg or diets containing MeHg-rich fish. In pregnant mice exposed to dietary MeHg, BtmerA/B decreases MeHg accumulation in the maternal liver, brain, placenta, and fetal brain, and attenuates the expression of cellular stress genes in the fetal brain. Overall, this work provides foundational proof-of-principle supporting the ability of an engineered gut bacterium to limit MeHg bioaccumulation and reduce adverse effects of chronic MeHg exposure.