Zhang Fuxin, Luan Jiahui, Suo Lijun, Wang Haiyan, Zhao Yi, Sun Tianyu, Ni Yawen, Cao Hongyun, Zou Xiaohui, Liu Bo
Department of Clinical Microbiology, Zibo City Key Laboratory of Respiratory Infection and Clinical Microbiology, Zibo City Engineering Technology Research Center of Etiology Molecular Diagnosis, Zibo Municipal Hospital, Zibo, China.
Department of Pulmonary and Critical Care Medicine, Zibo Municipal Hospital, Zibo, China.
Microbiol Spectr. 2025 Apr;13(4):e0263924. doi: 10.1128/spectrum.02639-24. Epub 2025 Mar 10.
Emerging evidence suggests that altered gut microbiota is linked to community-acquired pneumonia (CAP), but the potential mechanisms by which gut microbiota and its metabolites contribute to the development of CAP remain unclear. Fecal samples from 32 CAP patients and 36 healthy controls were analyzed through metagenomic sequencing and metabolomic profiling. The gut microbiota composition in CAP patients showed significant differences and lower diversity compared to healthy controls. Genera involved in short-chain fatty acid (SCFA) production, such as , , and , as well as species like , , , , and , were significantly depleted in CAP patients. Bacterial co-occurrence network analysis revealed an over-representation of pro-inflammatory bacteria, which contributed to the core gut microbiome in CAP patients. Metabolomic analysis of fecal samples identified a distinct metabolic profile, with a notable increase in arachidonic acid, but a decrease in secondary bile acids, such as deoxycholic acid, lithocholic acid, and ursodeoxycholic acid, compared to healthy controls. Spearman correlation analysis between differential microbiota and bile acids showed that , , , and were positively correlated with ursocholic acid, lithocholic acid, and ursodeoxycholic acid, respectively. Our results suggest that the reduction in secondary bile acids, insufficient production of SCFAs, and an overabundance of pro-inflammatory bacteria may contribute to metabolic inflammation in the body. These factors could play a key role in the pathogenesis of CAP, driven by gut microbiota alterations.
This study presents a comprehensive metagenomic and metabolomic analysis of fecal samples from community-acquired pneumonia (CAP) patients, identifying key characteristics, such as decreased secondary bile acids, imbalanced short-chain fatty acid production, and increased pro-inflammatory bacteria. These findings provide valuable insights into the mechanisms linking gut microbiota alterations to CAP pathogenesis and suggest that targeting the gut microbiota could be a promising strategy for intervening in CAP.
新出现的证据表明，肠道微生物群改变与社区获得性肺炎（CAP）有关，但肠道微生物群及其代谢产物促成CAP发生发展的潜在机制仍不清楚。通过宏基因组测序和代谢组学分析对32例CAP患者和36例健康对照者的粪便样本进行了分析。与健康对照相比，CAP患者的肠道微生物群组成存在显著差异且多样性较低。参与短链脂肪酸（SCFA）产生的属，如[此处原文缺失具体属名]、[此处原文缺失具体属名]和[此处原文缺失具体属名]，以及如[此处原文缺失具体种名]、[此处原文缺失具体种名]、[此处原文缺失具体种名]、[此处原文缺失具体种名]和[此处原文缺失具体种名]等物种，在CAP患者中显著减少。细菌共现网络分析显示促炎细菌过度存在，这构成了CAP患者肠道核心微生物群。粪便样本的代谢组学分析确定了一种独特的代谢谱，与健康对照相比，花生四烯酸显著增加，但次级胆汁酸如脱氧胆酸、石胆酸和熊去氧胆酸减少。差异微生物群与胆汁酸之间的Spearman相关性分析表明，[此处原文缺失具体菌名]、[此处原文缺失具体菌名]、[此处原文缺失具体菌名]和[此处原文缺失具体菌名]分别与熊去氧胆酸、石胆酸和熊去氧胆酸呈正相关。我们的结果表明，次级胆汁酸减少、SCFA产生不足以及促炎细菌过多可能导致体内代谢性炎症。这些因素可能在由肠道微生物群改变驱动的CAP发病机制中起关键作用。
本研究对社区获得性肺炎（CAP）患者的粪便样本进行了全面的宏基因组和代谢组分析，确定了关键特征，如次级胆汁酸减少、短链脂肪酸产生失衡和促炎细菌增加。这些发现为肠道微生物群改变与CAP发病机制之间的联系提供了有价值的见解，并表明针对肠道微生物群可能是干预CAP的一种有前景的策略。
