ArticleInfection and drug resistance2026
Analysis of Plasma Biomarkers and Potential Pathogenesis in Children with
Article in Infection and drug resistance, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Mycoplasma pneumoniae pneumonia (MPP) is a common cause of community-acquired pneumonia in children, yet its metabolic alterations and pathogenic mechanisms remain incompletely understood. This study aimed to characterize the plasma metabolomic profile of children with MPP and explore associated metabolic pathways. Methods: This retrospective case-control study involved 42 children including 14 MPP patients, 14 non-MPP (MPN) patients, and 14 healthy controls (HC). Clinical and laboratory data were compared across groups. Plasma metabolomic profiling was performed using liquid chromatography-tandem mass spectrometry (LC-MS/MS). Multivariate statistical analyses, including principal component analysis (PCA), partial least squares-discriminant analysis (PLS-DA), and orthogonal partial least squares-discriminant analysis (OPLS-DA), were employed to identify metabolic differences among groups. Pathway enrichment analysis used the KEGG and Reactome databases. Results: Clinically, the MPP group exhibited significantly higher C-reactive protein (CRP) levels and neutrophil percentages, and lower lymphocyte percentages (all P<0.05), indicating enhanced inflammatory response. Distinct plasma metabolic profiles were observed in the MPP group compared with the MPN and HC groups. A total of 127 differential metabolites were identified in MPP vs MPN, and 749 in MPP vs HC. Pathway enrichment analysis revealed that downregulated metabolites in MPP vs MPN were significantly enriched in the PPAR signaling pathway, linoleic acid metabolism, and vitamin digestion/absorption pathways. In MPP vs HC, downregulated metabolites were mainly enriched in amino acid metabolism (arginine biosynthesis, alanine-aspartate-glutamate metabolism), GABAergic synapse, and glycerophospholipid metabolism. These perturbations aligned with the enhanced inflammatory responses observed in MPP. Conclusion: Childhood MPP is characterized by extensive metabolic disturbances involving amino acid, lipid, vitamin, and neurotransmitter metabolism. These metabolic disturbances may be associated with altered antioxidant defense, inflammatory signaling and neuroimmune crosstalk in MPP. The identified metabolites and dysregulated pathways may represent preliminary exploratory candidate signatures that require further validation to establish their relevance to childhood MPP.
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