The effects of asthma on the oxidative stress, inflammation, and endothelial dysfunction in children with pneumonia
© 2022. The Author(s)..
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.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2022 |
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| Erschienen: |
2022 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:22 |
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| Enthalten in: |
BMC pediatrics - 22(2022), 1 vom: 08. Sept., Seite 534 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Shabestari, Ali Arjmand [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 13.09.2022 Date Revised 20.09.2022 published: Electronic Citation Status MEDLINE |
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| doi: |
10.1186/s12887-022-03596-5 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM345932765 |
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| 100 | 1 | |a Shabestari, Ali Arjmand |e verfasserin |4 aut | |
| 245 | 1 | 4 | |a The effects of asthma on the oxidative stress, inflammation, and endothelial dysfunction in children with pneumonia |
| 264 | 1 | |c 2022 | |
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| 500 | |a Date Completed 13.09.2022 | ||
| 500 | |a Date Revised 20.09.2022 | ||
| 500 | |a published: Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a © 2022. The Author(s). | ||
| 520 | |a 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 | ||
| 520 | |a 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 | ||
| 520 | |a 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) | ||
| 520 | |a CONCLUSIONS: Asthma can exacerbate the vascular dysfunction of pneumonia in children by increasing oxidative stress, inflammation, and endothelial dysfunction | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Asthma | |
| 650 | 4 | |a Community-acquired pneumonia | |
| 650 | 4 | |a Endothelial dysfunction | |
| 650 | 4 | |a Inflammation | |
| 650 | 4 | |a Oxidative stress | |
| 650 | 7 | |a Antioxidants |2 NLM | |
| 650 | 7 | |a Biomarkers |2 NLM | |
| 650 | 7 | |a Plasminogen Activator Inhibitor 1 |2 NLM | |
| 650 | 7 | |a Tumor Necrosis Factor-alpha |2 NLM | |
| 650 | 7 | |a Vascular Cell Adhesion Molecule-1 |2 NLM | |
| 700 | 1 | |a Imanparast, Fatemeh |e verfasserin |4 aut | |
| 700 | 1 | |a Mohaghegh, Pegah |e verfasserin |4 aut | |
| 700 | 1 | |a Kiyanrad, Habibeh |e verfasserin |4 aut | |
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