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Metabolomics Reveals Anaerobic Bacterial Fermentation and Hypoxanthine Accumulation for Fibrinous Pleural Effusions
Chih-Yung Chiu1,2, Mei-Ling Cheng3, Kin-Sun Wong1
1Division of Pediatric Pulmonology, Chang Gung Memorial Hospital at Linkou, College of Medicine , Chang Gung University , Taoyuan 333 , Taiwan.
Abstract:
Fibrin formation in infectious parapneumonic effusion (IPE) characterizes complicated parapneumonic effusion and is important for providing guidelines for the management of IPEs that require aggressive interventions. We aim to identify metabolic mechanisms associated with bacterial invasion, inflammatory cytokines, and biochemical markers in cases of fibrinous infectious pleural effusions in children with pneumonia. Pleural fluid metabolites were determined by 1H nuclear magnetic resonance spectroscopy. Metabolites that contributed to the separation between fibrinous and nonfibrinous IPEs were identified using supervised partial least squares discriminant analysis ( Q2/ R2 = 0.84; Ppermutation < 0.01). IL-1β in the inflammatory cytokines and glucose in the biochemical markers were significantly correlated with 11 and 9 pleural fluid metabolites, respectively, and exhibited significant overlaps. Four metabolites, including glucose, lactic acid, 3-hydroxybutyric acid, and hypoxanthine, were significantly correlated with plasminogen activator inhibitor type 1 in the fibrinolytic system enzymes. Metabolic pathway analysis revealed that anaerobic bacterial fermentation with increased lactic acid and butyric acid via glucose consumption and adenosine triphosphate hydrolysis with increased hypoxanthine appeared to be associated with fibrinous IPE. Our results demonstrate that an increase in lactic acid anaerobic fermentation and hypoxanthine accumulation under hypoxic conditions are associated with fibrin formation in IPE, representing advanced pleural inflammatory progress in children with pneumonia.
Insights
Fibrin formation in pediatric pneumonia effusions is linked to increased lactic acid and hypoxanthine. This suggests anaerobic fermentation and hypoxia drive advanced pleural inflammation in infectious parapneumonic effusions.
Area of Science:
- Biochemistry
- Microbiology
- Pediatric Pulmonology
Background:
- Fibrin formation in infectious parapneumonic effusion (IPE) indicates complicated disease requiring aggressive management.
- Understanding metabolic mechanisms in fibrinous IPEs is crucial for guiding treatment in pediatric pneumonia.
Purpose of the Study:
- To identify metabolic pathways associated with bacterial invasion, inflammatory cytokines, and biochemical markers in pediatric fibrinous IPEs.
- To correlate specific metabolites with inflammatory markers and fibrinolytic enzymes.
Main Methods:
- 1H nuclear magnetic resonance spectroscopy was used to analyze pleural fluid metabolites.
- Supervised partial least squares discriminant analysis differentiated between fibrinous and nonfibrinous IPEs.
- Correlation analysis linked metabolites to inflammatory cytokines (IL-1β), glucose, and plasminogen activator inhibitor type 1.
Main Results:
- Eleven metabolites correlated with IL-1β, and nine correlated with glucose, with significant overlap.
- Glucose, lactic acid, 3-hydroxybutyric acid, and hypoxanthine correlated with plasminogen activator inhibitor type 1.
- Metabolic analysis indicated anaerobic bacterial fermentation (lactic acid, butyric acid) and ATP hydrolysis (hypoxanthine) were associated with fibrinous IPE.
Conclusions:
- Increased lactic acid via anaerobic fermentation and hypoxanthine accumulation due to hypoxia are linked to fibrin formation in pediatric IPE.
- These metabolic changes signify advanced pleural inflammation in children with pneumonia and complicated effusions.
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