International immunopharmacology · 2023
Gut microbiota-derived autoinducer-2 regulates lung inflammation through the gut-lung axis.
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Zeng Xianghao, Yue Huawen, Zhang Ling, Chen Guimei, Zheng Qiao, Hu Qing, Du Xinhao, Tian Qian, Zhao Xinyu, Liang Lanfan, Yang Ziyi, Bai Hang, Liu Yanqin, Zhao Ming, Fu Xiangsheng
Аннотация
OBJECTIVE: This study aimed to determine whether autoinducer-2 (AI-2), a crucial bacterial metabolite and quorum sensing molecule, is involved in lung immunity through the gut-lung axis.
METHODS: The level of AI-2 and the gut microbiome composition were analysed in the stools from pneumonic patients and the mouse model of acute lung injury. The effect of AI-2 on lung inflammation was further investigated in the mouse model.
RESULTS: The diversity of the faecal microbiota was reduced in pneumonic patients treated with antibiotics compared with healthy volunteers. The AI-2 level in the stool was positively correlated with inflammatory molecules in the serum of pneumonic patients. Intraperitoneal injection of AI-2 reinforced lung inflammation in the acute lung injury mouse model, characterized by increased secretion of inflammatory molecules, including IL-6, IL-1β, C-C chemokines, and CXCL chemokines, which were alleviated by the AI-2 inhibitor D-ribose.
CONCLUSIONS: Our results suggested that gut microbiota-derived AI-2 could modulate lung inflammation through the gut-lung axis.
METHODS: The level of AI-2 and the gut microbiome composition were analysed in the stools from pneumonic patients and the mouse model of acute lung injury. The effect of AI-2 on lung inflammation was further investigated in the mouse model.
RESULTS: The diversity of the faecal microbiota was reduced in pneumonic patients treated with antibiotics compared with healthy volunteers. The AI-2 level in the stool was positively correlated with inflammatory molecules in the serum of pneumonic patients. Intraperitoneal injection of AI-2 reinforced lung inflammation in the acute lung injury mouse model, characterized by increased secretion of inflammatory molecules, including IL-6, IL-1β, C-C chemokines, and CXCL chemokines, which were alleviated by the AI-2 inhibitor D-ribose.
CONCLUSIONS: Our results suggested that gut microbiota-derived AI-2 could modulate lung inflammation through the gut-lung axis.