Microbiota-derived acetate enhances host antiviral response via NLRP3
Junling Niu,
Mengmeng Cui,
Xin Yang,
Juan Li,
Yuhui Yao,
Qiuhong Guo,
Ailing Lu,
Xiaopeng Qi,
Dongming Zhou,
Chenhong Zhang (),
Liping Zhao () and
Guangxun Meng ()
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Junling Niu: University of Chinese Academy of Sciences
Mengmeng Cui: University of Chinese Academy of Sciences
Xin Yang: Shanghai Jiao Tong University
Juan Li: University of Chinese Academy of Sciences
Yuhui Yao: University of Chinese Academy of Sciences
Qiuhong Guo: University of Chinese Academy of Sciences
Ailing Lu: University of Chinese Academy of Sciences
Xiaopeng Qi: Kunming Institute of Zoology, Chinese Academy of Sciences
Dongming Zhou: University of Chinese Academy of Sciences
Chenhong Zhang: Shanghai Jiao Tong University
Liping Zhao: Shanghai Jiao Tong University
Guangxun Meng: University of Chinese Academy of Sciences
Nature Communications, 2023, vol. 14, issue 1, 1-17
Abstract:
Abstract Pathogenic viral infections represent a major challenge to human health. Host immune responses to respiratory viruses are closely associated with microbiome and metabolism via the gut-lung axis. It has been known that host defense against influenza A virus (IAV) involves activation of the NLRP3 inflammasome, however, mechanisms behind the protective function of NLRP3 are not fully known. Here we show that an isolated bacterial strain, Bifidobacterium pseudolongum NjM1, enriched in the gut microbiota of Nlrp3−/− mice, protects wild-type but not Nlrp3 deficient mice against IAV infection. This effect depends on the enhanced production of type I interferon (IFN-I) mediated by NjM1-derived acetate. Application of exogenous acetate reproduces the protective effect of NjM1. Mechanistically, NLRP3 bridges GPR43 and MAVS, and promotes the oligomerization and signalling of MAVS; while acetate enhances MAVS aggregation upon GPR43 engagement, leading to elevated IFN-I production. Thus, our data support a model of NLRP3 mediating enhanced induction of IFN-I via acetate-producing bacterium and suggest that the acetate-GPR43-NLRP3-MAVS-IFN-I signalling axis is a potential therapeutic target against respiratory viral infections.
Date: 2023
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DOI: 10.1038/s41467-023-36323-4
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