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The effects of asthma on the oxidative stress, inflammation, and endothelial dysfunction in children with pneumonia
Ali Arjmand Shabestari1, Fatemeh Imanparast2,3, Pegah Mohaghegh1,4
1Department of Pediatrics, Amirkabir Hospital, Arak University of Medical Sciences, Arak, Iran.
Insights
Asthma worsens community-acquired pneumonia (CAP) in children by increasing oxidative stress, inflammation, and endothelial dysfunction. These findings highlight the significant impact of asthma on pneumonia severity and outcomes.
Area of Science:
- Pediatric Pulmonology
- Biomarkers of Inflammation and Oxidative Stress
- Vascular Endothelial Function
Background:
- Community-acquired pneumonia (CAP) is associated with pulmonary vascular endothelial dysfunction, inflammation, and oxidative stress.
- Asthma, a common chronic respiratory condition, may influence CAP outcomes, but the underlying mechanisms are not fully understood.
Purpose of the Study:
- To investigate the impact of asthma on biomarkers of oxidative stress, inflammation, and endothelial dysfunction in children with CAP.
- To compare these biomarkers between children with CAP and asthma, CAP alone, and healthy controls.
Main Methods:
- A cross-sectional study involving 75 children categorized into three groups: severe CAP with asthma, severe CAP alone, and healthy controls.
- Fasting blood samples were analyzed for serum malondialdehyde (MDA), total antioxidant capacity (TAC), tumor necrosis factor-alpha (TNF-α), soluble vascular cell adhesion molecule-1 (sVCAM-1), and plasminogen activator inhibitor-1 (PAI-1).
- Statistical comparison of anthropometric and biochemical parameters was performed using ANOVA and Tukey's post-hoc test.
Main Results:
- Children with CAP and asthma exhibited significantly lower TAC levels and higher MDA, TNF-α, sVCAM-1, and PAI-1 levels compared to healthy children and those with CAP alone.
- Children with CAP alone also showed significantly lower TAC levels and higher MDA, TNF-α, sVCAM-1, and PAI-1 levels compared to healthy controls.
- Biomarkers of endothelial dysfunction (sVCAM-1 and PAI-1) were significantly elevated in both CAP groups compared to healthy controls, with higher levels observed in the CAP with asthma group.
Conclusions:
- Asthma exacerbates the vascular dysfunction associated with pneumonia in children.
- The exacerbation is mediated by increased oxidative stress, inflammation, and endothelial dysfunction.
- These findings underscore the complex interplay between asthma and CAP, impacting disease severity and clinical outcomes.
Background:
In community-acquired pneumonia (CAP), pulmonary vascular endothelial dysfunction, inflammation, and oxidative stress (OS) are prominent and interesting as the unfavorable clinical outcomes of it. Asthma as a common chronic respiratory disease may affect the clinical outcomes of pneumonia, but the exact mechanism of this effect remains unclear. The present study aimed to assess the effects of asthma on the OS, inflammation, and endothelial dysfunction biomarkers in the children pneumonia.
Methods:
A cross-sectional study designed with a total of 75 children including both severe CAP and asthma (as group I), severe CAP alone (as group II), and healthy children (as group III) was conducted. Fasting blood samples were taken to the assay of serum malondialdehyde (MDA), total antioxidant capacity (TAC), tumor necrosis factor-alpha (TNF-α), soluble vascular cell adhesion molecule-1 (sVCAM-1), and plasminogen activator inhibitor-1 (PAI-1). The mean of anthropometric and biochemical parameters was compared by ANOVA and Tukey post-hoc test between groups.
Results:
We observed TAC levels in groups I and II (0.997 ± 0.22 and 1.23 ± 0.21 mmol/l, respectively) were significantly lower compared with group III (1.46 ± 0.19 mmol/l, P value < 0.001). It was significantly higher in group II than in group I (P value < 0.001). Also, we observed MDA and TNF-α levels in groups I (6.94 ± 1.61 μmol/l, 7.34 ± 2.23 pg/ml, respectively) and II (2.57 ± 0.40 μmol/l, 5.54 ± 1.84 pg/ml, respectively) were significantly higher compared with group III (1.89 ± 0.27 μmol/l, 3.42 ± 1.32 pg/ml, P value < 0.001, P value < 0.001, respectively). VCAM-1 and PAI-1 levels as the endothelial dysfunction biomarkers were significantly higher in group I (1.5 ± 0.62 mmol/l, 10.52 ± 3.2 AU/ml, respectively) compared with groups II (1.06 ± 0.53 mmol/l and 8.23 ± 3.4 AU/ml; P value < 0.001, P value < 0.001, respectively) and III (0.6 ± 0.35 mmol/l and 2.39 ± 0.83 AU/ml; P value < 0.001, P value < 0.001, respectively). Also, VCAM-1 and PAI-1 levels were significantly higher in group II compared with groups III (P value < 0.001, P value < 0.001).
Conclusions:
Asthma can exacerbate the vascular dysfunction of pneumonia in children by increasing oxidative stress, inflammation, and endothelial dysfunction.
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