Gut bacteria alleviate smoking-related NASH by degrading gut nicotine

Bo Chen, Lulu Sun, Guangyi Zeng, Zhe Shen, Kai Wang, Limin Yin, Feng Xu, Pengcheng Wang, Yong Ding, Qixing Nie, Qing Wu, Zhiwei Zhang, Jialin Xia, Jun Lin, Yuhong Luo, Jie Cai, Kristopher W. Krausz, Ruimao Zheng, Yanxue Xue, Ming-Hua Zheng (), Yang Li (), Chaohui Yu (), Frank J. Gonzalez () and Changtao Jiang ()
Additional contact information
Bo Chen: Peking University
Lulu Sun: National Institutes of Health
Guangyi Zeng: Peking University
Zhe Shen: The First Affiliated Hospital, College of Medicine, Zhejiang University
Kai Wang: Peking University
Limin Yin: Fudan University
Feng Xu: Peking University
Pengcheng Wang: Peking University
Yong Ding: Peking University
Qixing Nie: Peking University
Qing Wu: Peking University
Zhiwei Zhang: Peking University
Jialin Xia: Peking University
Jun Lin: Peking University
Yuhong Luo: National Institutes of Health
Jie Cai: National Institutes of Health
Kristopher W. Krausz: National Institutes of Health
Ruimao Zheng: Peking University
Yanxue Xue: Peking University
Ming-Hua Zheng: The First Affiliated Hospital of Wenzhou Medical University
Yang Li: Fudan University
Chaohui Yu: The First Affiliated Hospital, College of Medicine, Zhejiang University
Frank J. Gonzalez: National Institutes of Health
Changtao Jiang: Peking University

Nature, 2022, vol. 610, issue 7932, 562-568

Abstract: Abstract Tobacco smoking is positively correlated with non-alcoholic fatty liver disease (NAFLD)1–5, but the underlying mechanism for this association is unclear. Here we report that nicotine accumulates in the intestine during tobacco smoking and activates intestinal AMPKα. We identify the gut bacterium Bacteroides xylanisolvens as an effective nicotine degrader. Colonization of B. xylanisolvens reduces intestinal nicotine concentrations in nicotine-exposed mice, and it improves nicotine-exacerbated NAFLD progression. Mechanistically, AMPKα promotes the phosphorylation of sphingomyelin phosphodiesterase 3 (SMPD3), stabilizing the latter and therefore increasing intestinal ceramide formation, which contributes to NAFLD progression to non-alcoholic steatohepatitis (NASH). Our results establish a role for intestinal nicotine accumulation in NAFLD progression and reveal an endogenous bacterium in the human intestine with the ability to metabolize nicotine. These findings suggest a possible route to reduce tobacco smoking-exacerbated NAFLD progression.

Date: 2022
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DOI: 10.1038/s41586-022-05299-4

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