Frontiers in cellular and infection microbiology · 2026
Longitudinal multi-omics evidence reveals lung injury and concurrent disruption of intestinal flora and serum metabolism by cigarette smoke and influenza virus.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Liu Zhihang, Li Huameng, Xiang Yuting, Ren Shaocong, Pan Wenchao, Ling Zihan, Dong Jianling, Liang Ziyao, Quan Jingyu, Fan Long, Lin Lin, Wu Lei, Yu Xuhua
Аннотация
BACKGROUND: Cigarette smoke (CS) exposure is the primary risk factor for chronic obstructive pulmonary disease (COPD), and respiratory viral infections, particularly influenza A virus (IAV), are major triggers of acute exacerbations of COPD (AECOPD). However, the dynamic interactions among pulmonary pathology, gut microbiota, and host metabolism during these episodes remains unclear. This study aimed to delineate the longitudinal characteristics of virus-induced AECOPD and identify potential biomarkers.
METHODS: Mice were exposed to cigarette smoke for eight weeks, followed by intranasal inoculation with IAV. A longitudinal assessment was conducted from day 1 to day 15 post-infection, integrating analyses of lung pathology, lung function, gut microbiome, and both serum and fecal metabolomes. Additionally, random forest modeling was employed to identify specific metabolic biomarkers associated with the acute exacerbation stage.
RESULTS: Mice exposed to cigarette smoke and IAV exhibited significant pulmonary immune cell recruitment, impaired lung function, and emphysematous changes, peaking at day 5 post-infection. By day 15, acute airway inflammation had subsided; however, interstitial immune cell infiltration, collagen deposition, and emphysema persisted. 16S rRNA sequencing revealed dynamic shifts in gut microbiota composition, with the abundance of Intestinimonas positively correlating with pulmonary inflammatory markers. Untargeted metabolomics demonstrated sustained downregulation of serum unsaturated fatty acid biosynthesis pathways from day 3 to day 15, and these metabolites were negatively correlated with lung inflammation. Random forest analysis identified 1-Methylnicotinamide (1-MNA) as a promising biomarker for distinguishing virus-triggered AECOPD, achieving an area under the curve (AUC) of 1.0.
CONCLUSION: This study demonstrates that cigarette smoke combined with influenza infection induces persistent lung injury alongside concurrent disruption of intestinal flora and serum metabolism. The findings show that gut microbiota and metabolites are potential biomarkers and supplementation with unsaturated fatty acids may represent a novel therapeutic strategy for virus-induced AECOPD.
METHODS: Mice were exposed to cigarette smoke for eight weeks, followed by intranasal inoculation with IAV. A longitudinal assessment was conducted from day 1 to day 15 post-infection, integrating analyses of lung pathology, lung function, gut microbiome, and both serum and fecal metabolomes. Additionally, random forest modeling was employed to identify specific metabolic biomarkers associated with the acute exacerbation stage.
RESULTS: Mice exposed to cigarette smoke and IAV exhibited significant pulmonary immune cell recruitment, impaired lung function, and emphysematous changes, peaking at day 5 post-infection. By day 15, acute airway inflammation had subsided; however, interstitial immune cell infiltration, collagen deposition, and emphysema persisted. 16S rRNA sequencing revealed dynamic shifts in gut microbiota composition, with the abundance of Intestinimonas positively correlating with pulmonary inflammatory markers. Untargeted metabolomics demonstrated sustained downregulation of serum unsaturated fatty acid biosynthesis pathways from day 3 to day 15, and these metabolites were negatively correlated with lung inflammation. Random forest analysis identified 1-Methylnicotinamide (1-MNA) as a promising biomarker for distinguishing virus-triggered AECOPD, achieving an area under the curve (AUC) of 1.0.
CONCLUSION: This study demonstrates that cigarette smoke combined with influenza infection induces persistent lung injury alongside concurrent disruption of intestinal flora and serum metabolism. The findings show that gut microbiota and metabolites are potential biomarkers and supplementation with unsaturated fatty acids may represent a novel therapeutic strategy for virus-induced AECOPD.