Table 2_Metabolomic analysis of Streptococcus pneumoniae: uncovering key metabolic pathways.xlsx

BackgroundPneumococcal infection, caused by Streptococcus pneumoniae, is a prevalent cause of community-acquired pneumonia and a major pathogen responsible for illnesses such as meningitis, sepsis, and pharyngitis. The complex etiology of S. pneumoniae infection poses significant challenges in elucidating the molecular mechanisms underlying its pathogenesis.
MethodsIn this study, twenty serum samples from individuals infected with S. pneumoniae and fifteen serum samples from normal controls were analyzed using liquid chromatography/mass spectrometry (LC–MS) to identify metabolites. Multivariate statistical analyses, including principal component analysis (PCA) and orthogonal partial least squares discriminant analysis (OPLS-DA), were used to identify potential metabolites. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis was employed to map the metabolic pathways associated with these metabolites.
ResultsThrough comparative analysis of the metabolic profiles of infected individuals and normal controls, we identified 418 metabolites that significantly contributed to the differentiation of group samples. The identified metabolites were categorized into various groups, such as amino acids, fatty acids, and phosphatidylcholine, and were enriched in pathways including galactose metabolism, the hypoxia-inducible factor-1 (HIF-1) signaling pathway, the citrate cycle, the pentose phosphate pathway, and glycolysis/gluconeogenesis. S. pneumoniae infection induced significant variations in the serum metabolome, with activation of metabolic pathways implicated in the immune response.
ConclusionOur study provides a comprehensive and real-time analysis of the metabolic network, elucidating the complex processes that occur following pathogen invasion in the human body. The identification of metabolic biomarkers and enriched pathways lays a foundational framework for research and offers visualizable targets for the diagnosis and treatment of pneumococcal infections.

背景：由肺炎链球菌（Streptococcus pneumoniae）引发的感染是社区获得性肺炎的常见致病原因，同时也是脑膜炎、败血症、咽炎等多种疾病的主要致病菌。肺炎链球菌感染的复杂病因学机制，为阐明其发病的分子机制带来了显著挑战。
方法：本研究采用液相色谱-质谱联用（liquid chromatography/mass spectrometry，LC-MS）技术，对20份肺炎链球菌感染患者的血清样本与15份正常对照血清样本进行代谢物检测。通过主成分分析（Principal Component Analysis，PCA）、正交偏最小二乘判别分析（Orthogonal Partial Least Squares Discriminant Analysis，OPLS-DA）等多元统计分析方法筛选潜在差异代谢物，并采用京都基因与基因组百科全书（Kyoto Encyclopedia of Genes and Genomes，KEGG）通路富集分析，对这些代谢物所关联的代谢通路进行映射注释。
结果：通过对比感染患者与正常对照人群的血清代谢谱，本研究共鉴定得到418个可显著区分两组样本的代谢物。这些鉴定出的代谢物可分为氨基酸、脂肪酸、磷脂酰胆碱等多个类别，其富集通路涵盖半乳糖代谢、缺氧诱导因子-1（hypoxia-inducible factor-1，HIF-1）信号通路、三羧酸循环、磷酸戊糖途径以及糖酵解/糖异生过程。肺炎链球菌感染可显著改变血清代谢组特征，且与免疫应答相关的代谢通路呈现激活状态。
结论：本研究对感染后的代谢网络进行了全面且实时的分析，阐明了病原体侵入人体后发生的复杂生理过程。本研究鉴定得到的代谢生物标志物与富集代谢通路，为肺炎链球菌感染的相关研究奠定了基础框架，同时也为该类感染的诊断与治疗提供了可视化的靶向目标。