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Rifaximin ameliorates influenza A virus infection-induced lung barrier damage by regulating gut microbiota

文献类型： 外文期刊

作者： Zhang, Yijia 1 ; Chen, Yafei 1 ; Xia, Jun 2 ; Li, Li 1 ; Chang, Lifeng 1 ; Luo, Haowei 1 ; Ping, Jihui 3 ; Qiao, Wenna 1 ; Su, Juan 1 ;

作者机构： 1.Nanjing Agr Univ, Coll Vet Med, Lab Anim Neurobiol, Nanjing 210095, Peoples R China

2.Xinjiang Acad Anim Sci, Inst Vet Med, Urumqi 830013, Peoples R China

3.Nanjing Agr Univ, Coll Vet Med, MOE Joint Int Res Lab Anim Hlth & Food Safety, Engn Lab Anim Immun Jiangsu Prov, Nanjing 210095, Peoples R China

关键词： Rifaximin; Influenza A virus; Tryptophan metabolism; ILC3 cell; Gut-lung axis

期刊名称：APPLIED MICROBIOLOGY AND BIOTECHNOLOGY （ 影响因子：4.3； 五年影响因子：5.1 ）

ISSN： 0175-7598

年卷期： 2024 年 108 卷 1 期

页码：

收录情况： SCI

摘要： Prior research has indicated that the gut-lung-axis can be influenced by the intestinal microbiota, thereby impacting lung immunity. Rifaximin is a broad-spectrum antibacterial drug that can maintain the homeostasis of intestinal microflora. In this study, we established an influenza A virus (IAV)-infected mice model with or without rifaximin supplementation to investigate whether rifaximin could ameliorate lung injury induced by IAV and explore the molecular mechanism involved. Our results showed that IAV caused significant weight loss and disrupted the structure of the lung and intestine. The analysis results of 16S rRNA and metabolomics indicated a notable reduction in the levels of probiotics Lachnoclostridium, Ruminococcaceae_UCG-013, and tryptophan metabolites in the fecal samples of mice infected with IAV. In contrast, supplementation with 50 mg/kg rifaximin reversed these changes, including promoting the repair of the lung barrier and increasing the abundance of Muribaculum, Papillibacter and tryptophan-related metabolites content in the feces. Additionally, rifaximin treatment increased ILC3 cell numbers, IL-22 level, and the expression of ROR gamma and STAT-3 protein in the lung. Furthermore, our findings demonstrated that the administration of rifaximin can mitigate damage to the intestinal barrier while enhancing the expression of AHR, IDO-1, and tight junction proteins in the small intestine. Overall, our results provided that rifaximin alleviated the imbalance in gut microbiota homeostasis induced by IAV infection and promoted the production of tryptophan-related metabolites. Tryptophan functions as a signal to facilitate the activation and movement of ILC3 cells from the intestine to the lung through the AHR/STAT3/IL-22 pathway, thereby aiding in the restoration of the barrier.

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